Online Higher Education In UAE Essay Example | Topics and Well Written Essays - 3000 words

Online Higher Education In UAE - Essay Example The study aimed to evaluate on general overview of E learning in UAE learning institutions.Based on the collected data from the UAE students and staffs, the information will assist the institutions to understand on the barriers affecting adaptation of the E learning system. The higher learning institutions can then begin to analyze on how to combat the challenges at their disposal. The institutions can assess the source of the faculty and students’ negative attitudes in order formulate effective measures like online games or training to alleviate the issue. The institutions can also evaluate which course programs or courses have high E learning registrations to expand their acceptability. The UAE government can also utilize the information to assess the challenges students and higher learning institutions face while using the E learning system to formulate ways of promoting its user-ability and popularity within its borders. The system being expensive to implement, the UAE gov ernment can chip in through offering free technical training or subsidies to spearhead its adaptation among higher learning institutions. This paper makes a conclusion that one of the limitations that the study is likely to face is completion irregularities of the online questionnaire. Most of the students and staffs are normally occupied or busy where they may ignore the questionnaires. Some of the questionnaires can also be returned late, hence hindering the research.

Accent Strength And Regional Accents

Accent Strength And Regional Accents At a party one night a visitor from another country remarks that You dont have so strong an accent as your friends. You had previously believed that you had no accent and that you spoke like your friends, but the statement helps you to realize that you carry a regional accent, just like everyone else around you. What explanation could you offer your visitor for why you never realized that fact before and why you really do have an accent just like the one your friends have? What explanation could you offer your visitor for why you never realized that fact before? What explanation could you offer your visitor for why you really do have an accent just like the one your friends have? 1) Why I never realised that: a) I had no accent. b) My accent is not as strong as my friends. c) I have an accent just like one of my friends. WHY I NEVER REALISED THAT I HAD AN ACCENT. Most people dont realize that they have an accent because they are accustom to the pronunciation and rhythm of speech in their country. It sounds normal hearing other Trinidadian speak. Whenever I meet foreigners, it intrigues me to hear their accent and I try to figure out which country they are from. Hearing a foreigners accent sounds strange to me because it is not the norm in my place of abode. Although most people have an accent they do not acknowledge this greatly. We live in a society where mostly everyone speaks and sounds the same, with the exception of foreigners and those with speak difficulties. We always consider the main accent as normal and any other accent as funny or strange. I never realized this because I lived my entire in Trinidad and never travelled or lived abroad where my accent was not the popular. Hearing you speak to me makes me realize that the way I speak CUNNING LINGUISTICS Everyone has an accent. Some readers might think, No shit! Thats obvious! But its not obvious, smart arse. A survey held in Britain in 2005 revealed that 7% of respondents dont believe they have an accent. I would claim that the actual figure is even much higher than that. Were all prisoners of our own culture. Living within a society, were surrounded and bombarded by a majority accent. To us, that accent sounds natural and other accents sound different. Sometimes we confuse the familiar accent as being right, and the different ones as being wrong. It may sound silly, but I never realised I had an accent until I set foot in England at age 25. Having lived in Trinidad for my whole life, to me when Trinis spoke it sounded normal. But in England, as soon as I said something people would look at me. The funny thing too is that I had to learn what my accent sounded like by listening to my other Trini friends, and still I didnt think they had an accent. Then I realised I had to listen to intonations of how Trinidadians spoke. Some people change their accents to blend in. However, I think my accent got even thicker, as my way to hold on to my Caribbean identity, and I revelled in speaking Trinidadian Creole (which is a dialect that was formed by slaves mixing English with their own language, and includes unique words and sayings). People say Trinidadians accent sounds happy. To quote a previous boss, she said it sounded like a lilt. When I speak Standard English people understand it quite well. Like Paull says, it depends on how its delivered; its the slang/ dialect that can confuse people. Ive spoken with Paull, and another Aussie and had no problems understanding them. Seems they understood me quite well also, and our accents are quite different. Ask A Linguist FAQ What is an accent? An accent is a way of pronouncing a language. It is therefore impossible to speak without an accent. Some people may think they do not have an accent. Or you may think that there are other people who do not have an accent. Everyone has an accent. The term accentless is sometimes used (by non-linguists) about people who speak one of the high prestige reference accents (such as General American or, less commonly, RP), which are associated with people from a fairly wide region and with people of high social class. But these are also accents. I will mention them again later in this FAQ. MY ACCENT IS NOT AS STRONG AS MY FRIENDS CUNNING LINGUISTICS Accents dont just vary at the level of nationality (e.g., Aussie) or region (e.g., Boston). They also vary with the individual (e.g., you). Your accent is a fingerprint, a totally unique, distinctive way of talking (linguists call this an idiolect). It isnt fixed though. It can change, with the right combination of influence and interest. Recently, some twit asked me, Why dont you sound American yet? Okay, Ive been in the States for two and a half years now, and my accent now sounds a little different to me. But, by contrast, this difference is generally imperceptible to Americans (and non-linguists). Your accent does leave a Hansel and Gretel-like trail of where youve been. Obviously, it takes awhile for a new accent to kick in. Other factors can influence this process too, whether you want to adopt an accent (convergence) or dont want to adopt it (divergence). Accents are like tracking devices that can reveal where youve been. The field of Forensic Linguistics investigates this area. In August 2005, a militant video of an al-Qaeda fighter was found. A forensic linguist was able to determine several aspects of the fighters identity, that he had been raised in Australia and possibly had parents of Middle Eastern descent. This area is useful in legal cases, especially for identification, transcription and in authenticating recordings. Accent (linguistics) Prestige Certain accents are perceived to carry more prestige in a society than other accents. This is often due to their association with the elite part of society. For example in the United Kingdom, Received Pronunciation of the English language is associated with the traditional upper class. I HAVE AN ACCENT JUST LIKE ONE OF MY FRIENDS CUNNING LINGUISTICS Another twit drives around with a bumper sticker on his SUV proclaiming: Welcome to America. Nowà ¢Ã¢â€š ¬Ã‚ ¦speak English or get out! What a funny fuck! This pseudo-patriotic, prejudiced twit has no control over who speaks what and where. This is a dynamic process that he can only witness. American English may be the fastest growing version of Englishà ¢Ã¢â€š ¬Ã‚ ¦but Spanish is the fastest growing language in Americaà ¢Ã¢â€š ¬Ã‚ ¦ So, accents can reveal our regional origins, but they can also suggest what kind of social circles we move in. Compare the Queen of Englands accent to that of a miner in Yorkshire. Accent can also provide info about your economic background and education. Stop practicing your accentà ¢Ã¢â€š ¬Ã‚ ¦I can hear you right now! Accent (linguistics) As human beings spread out into isolated communities, stresses and peculiarities develop. Over time these can develop into identifiable accents. In North America, the interaction of people from many ethnic backgrounds contributed to the formation of the different varieties of North American accents. It is difficult to measure or predict how long it takes an accent to formulate. Accents in the USA, Canada and Australia, for example, developed from the combinations of different accents and languages in various societies, and the effect of this on the various pronunciations of the British settlers, yet North American accents remain more distant, either as a result of time or of external or foreign linguistic interaction, such as the Italian accent. In many cases, the accents of non-English settlers from Great Britain and Ireland affected the accents of the different colonies quite differently. Irish, Scottish and Welsh immigrants had accents which greatly affected the vowel pronunciation of certain areas of Australia and Canada Social factors When a group defines a standard pronunciation, speakers who deviate from it are often said to speak with an accent. People from the United States would speak with an accent from the point of view of an Australian, and vice versa. Accents such as BBC English or General American may sometimes be erroneously designated in their countries of origin as accentless to indicate that they offer no obvious clue to the speakers regional background. Groups sharing an identifiable accent may be defined by any of a wide variety of common traits. An accent may be associated with the region in which its speakers reside (a geographical accent), the socio-economic status of its speakers, their ethnicity, their caste or social class, their first language (when the language in which the accent is heard is not their native language), and so on. Regional accents of English Local accents are part of local dialects. Any dialect of English has unique features in pronunciation, vocabulary, and grammar. The term accent describes only the first of these, namely, pronunciation. See also: List of dialects of the English language. Non-native speakers of English tend to carry over the intonation and phonemic inventory from their mother tongue into their English speech. For more details see Non-native pronunciations of English. Among native English speakers, many different accents exist. Some regional accents are easily identified by certain characteristics. Further variations are to be found within the regions identified below; for example, towns located less than 10 miles (16 km) from the city of Manchester such as Bolton, Oldham and Salford, each have distinct accents, all of which form the Lancashire accent, yet in extreme cases are different enough to be noticed even by a non-local listener. There is also much room for misunderstanding between people from different regions, as the way one word is pronounced in one accent (for example, petal in American English) will sound like a different word in another accent (for example, pearl in Scottish English). Your accent results from how, where, and when you learned the language you are speaking and it gives impressions about you to other people. People do not have a single fixed accent which is determined by their experiences. We can control the way we speak, and do, both consciously and unconsciously. Most people vary their accent depending on who they are speaking with. We change our accents, often without noticing, as we have new life experiences. How accurate people are in knowing about you from your accent depends not only on the features of your accent, but also on who the listener is, and what they know about the other people who speak with a similar accent to you. Your accent might be one that is associated with people from a particular place (for example, with being from New York, London, or Delhi). Some people might just hear you as simply being from the US, England, or India. Your accent might give the impression that you spoke some other language before the one you are speaking at the moment (you might speak French with an English accent, or English with a Korean accent). Its impossible to speak without conveying some information through your accent. All languages are spoken with several different accents. There is nothing unusual about English. And not everyone who comes from the same place speaks the same: in any place there is a variety of accents. Language changes over time. We get new words, there are grammatical changes, and accents change over time. If you listen to recordings made by people from your own language community 100 years ago, you will hear for yourself that even over that time accents have changed. Try out some of the links from the Spoken Word Archive Group , for example. Why do languages develop different accents? Human nature. In all sorts of ways, we behave like those we mix with. We are members of social groups, and within our social group we like to behave in similar ways and show that we belong. We do this in language as well as in other ways (e.g. what we wear, what we eat). When groups become distinct, the way they speak becomes distinct too. This happens socially and geographically, but is easiest to illustrate by geographical differences. If a single group splits into two (imagine that one half goes to Island A and one half to Island B), then once they have separated, their accents will change over time, but not in the same way, so that after just one generation the accent of Island A will be different from the accent of Island B. If they stay completely separated for centuries, their dialects may become so different that we will start wanting to say they are speaking two different languages. Why are the accents a particular place like they are? Separate development accounts for some accent variation. But sometimes we need to talk about the first generation of speakers of a particular language brought up in a new place. The first children to grow up in a new place are very important. The children who grow up together are a peer group. They want to speak the same as each other to express their group identity. The accent they develop as they go through their childhood will become the basis for the accents of the new place. So where does their accent come from? The first generation of children will draw on the accents of the adults around them, and will create something new. If people move to a new place in groups (as English speakers did to America, Australia and New Zealand) that group usually brings several different accents with them. The children will draw on the mixture of accents they hear and create their own accent out of what they hear. The modern accents of Australia are more similar to London accents of English than to any other accent from England this is probably because the founder generation (in the eighteenth century) had a large component drawn from the poor of London, who were transported to Australia as convicts. The accents of New Zealand are similar to Australian accents because a large proportion of the early English-speaking settlers of New Zealand came from Australia. The mix found in the speech of the settlers of a new place establishes the kind of accent that their children will develop. But the first generation born in the new place will not keep the diversity of their parents generation they will speak with similar accents to the others of their age group. And if the population grows slowly enough, the children will be able to absorb subsequent children into their group, so that even quite large migrations of other groups (such as Irish people into Australia) will not make much difference to the accent of the new place. Most parents know this. If someone from New York (US) marries someone from Glasgow (Scotland, UK), and these two parents raise a child in Leeds (England, UK), that child will not speak like either of the parents, but will speak like the children he (I know of such a child!) is at school with. About Accents By Shiromi Nassreen, eHow Contributor When we hear a voice, one of the first things we might notice is a persons accent, particularly if that accent happens to be different from our own. If we cant see the person, we may even come to conclusions based on the accent. Accents can give us perceptions about a person that are not always accurate, such as how intelligent the person is or how much money he makes. What is an Accent? 1. An accent is the way in which a person pronounces a word in a language. Accents are caused by a number of factors, primarily the region that someone is from, where he learned to speak the language and his social background. However, despite that fact that accents tend to give away information regarding a persons background, accents can be changed. In fact, people will often unknowingly change their accents to fit their current location and social group. Some believe that they dont have an accent because it is a more commonly known accent such as the General American accent or the British Received Pronunciation typically seen on television; however, it is still an accent. The Origin of Accents 2. Accents develop and change naturally over time. However, a primary cause for the changing of an accent is when groups of people migrate to new locations. People will usually speak with the same accent as their peers. This helps to create a group identity. When groups migrate, such as the settlers of North America, they find themselves among a group where a variety of languages and accents is being spoken. The children of that group will draw on the accents spoken around them and develop a new accent. Accents and Development 3. Accents are often developed during childhood. Generally, children often find it easier to pick up accents. If a child whose parents are from England moves to Australia, the child is unlikely to speak with an English accent, speaking instead with the accent of the childs peers. However, should the child as an adult later wish to change her accent, that is also possible. Accents and Social Factors 4. Accents can not only indicate a region that a person is from but also that persons social background. Often certain accents are stereotypically associated with a certain class. British Received Pronunciation is usually associated with the upper class and a well-educated person. According to a study at Bath Spa University, the Brummie accent of Birmingham is thought to be the least intelligent of all the British regional accents studied. However, a person unfamiliar with these stereotypesan American, for examplewould not have the same perceptions of the accent.

Cinnamon: Its Not Just For Making Cinnamon Rolls :: Botany

Cinnamon: It's Not Just For Making Cinnamon Rolls Most people around the world are familiar with the sweet and pungent taste of cinnamon. Cinnamon is the common name for the trees and shrubs that belong to the genus Cinnamomum of the Laurel family (Lauraceae). Cinnamon spice comes primarily from the Sri Lankan cinnamon known as Cinnamomum zeylanicum. It is obtained from the plant by drying the central part of the bark, which is then sold in stick or powdered form. The cinnamon oil is extracted from the waste products of drying and the pointed black fruits that the tree bears (1). This oil is used for medicinal purposes or flavoring (2). Cinnamomum Zeylanicum is the source of cinnamon that we in the United States commonly buy. Cinnamon contains cinnamic aldehyde, essential oils, Eugenol, metholeugenol, muscilage, sucrose, starch, and tannin (3). Distribution Have you ever wondered where cinnamon comes from? It is unbelievable to think that there is a place somewhere in the world where cinnamon is commonly seen growing along the side of the road. Just imagine walking through campus with cinnamon trees growing all around you. Cinnamon is native to India, Mayala, Ceylon, China, Japan and Taiwan, where it is as common to them as an Oak tree wood be to us (1). The spice grows in a number of tropical forests and is extensively cultivated throughout the tropical regions of the world, including Madagascar, Brazil, and the Caribbean (4). Cinnamomum zeylanicum, True Cinnamon is native to Sri Lanka, India, where it was one of the spices responsible for world trade (5). Description The Cinnamomum zeylanicum tree grows up to thirty feet tall with ovate to ovate-lanceolate leaves that can be four to seven inches long. The flowers are inconspicuous, and the panicles of the yellowish flowers are usually longer than the leaves (6). These panicles bear pointed black fruits from which cinnamon oil is extracted. The cinnamon sticks are made from the bark of the tree and are rolled naturally when the bark is sun-dried. The tree grows best in deep, well-drained, moist soils (1). Uses Cinnamon (Cinnamomum zeylanicum) has many common everyday uses and some not so common uses. Everybody has probably used cinnamon for some reason, whether for cooking purposes or medicinal purposes. Despite being widely used in food and pharmacy it is also important in the cosmetic and perfumery industries (7). In some areas cinnamon has been known to be used for religious purposes.

Water, the Finite Resources

Water, The Finite Resources Outline I. Introduction A. Opener: What is water scarcity? B. Thesis statement: One of the crises that our environment is facing is fresh water scarcity which is a very serious issue and it affects our global environmental. II. Water shortage effects on environment and human beings. A. Causes disease B. Agricultural fields C. Poverty group D. Aquatic Ecosystems III. Water scarcity is causes by different factors. A. Global warming B. Changes of climate C. Decreasing ground water level D. Population growth and the increased consumption of water IV. Solution for water scarcity is a necessity. A.Water Sharing Treaty B. Environmentalists Oppose Desalination Solution C. Government’s rules, regulations and plan V. Conclusion: People should use water wisely to prepare a better future for our next generation. Water, Our Finite Resources One of the crises that our environment is facing is fresh water scarcity which is a very serious issue and it affects our g lobal environment. In the boundless black desert of space, the Earth which is always a blue-green oasis has a finite stock of fresh water (Lean, 2009). Water is the principal element for all socio-economic growth and for sustaining healthy ecosystems (â€Å"Water scarcity: The†, n. . ). Water scarcity is the product of an inequity between the supply of and demand for water supplies in a geographical area. Plainly put, water scarcity is based on the lack of water which means the quantity of water and the lack of access to safe water which refers to quality of the water. It is hard to picture that safe and clean water cannot be taken for granted; but, finding a dependable source of safe water consumes time and it is expensive in the developing world. This is defined as economic scarcity whereas physical scarcity of water can be overcome if more water can be found, but it needs more resources to do it.In other areas, the shortage of water is a more intense problem (FOA, n. d. ). There is only less than 1% of the world’s fresh water which is readily accessible for direct human use (â€Å"Water facts†, n. d. ). Lean (2009) researched that by 2030, more than half of the world’s population will stay in high risk areas. Based on the World Water Development report, which is compiled by 24 UN agencies under the auspices of UNESCO, add that shortages of water are starting to constrain the economic growth in regions as diverse as Australia, California, Chia, India, and Indonesia (FOA, n. d. ).Thus, this can show that water scarcity really affects human beings and the environment especially poverty, agriculture field, aquatic ecosystems, and causes disease. Poverty is the largest issue on which water crisis has an impact. Shah (2010) announced that there are 2. 6 billion people in the world who lack basic sanitation whereas inadequate access to water has affected 1. 1 billion people in developing countries, while the rest of world enjoys direct access to freshwater for domestic use. For poor people, water scarcity is about ensuring the fair and safe access which they need to secure their livelihoods, and sustain their lives. FOA, n. d. ). About 1. 8 billion people only can access water within one kilometer and consume around twenty liters per day; people in United Kingdom use on average 150liters per day. One out of every five children (400 million) from the developing world does not have access to safe water. Around 443 million children lost their school days each year from water-related illness (Shah, 2010). Furthermore, lack of water means millions of women are spending many hours every day in collecting water, sometimes from several miles away (FOA, n. d. ).It is clearly show that water scarcity is preventing them from attaining even first step on the socioeconomic ladder. Water scarcity has a huge influence on agriculture fields and food production. (Sentlinger, n. d. ) Since agriculture is the biggest water consumer, it takes 70percent of the total use; water deficiency causes weak farming harvest, loss of animal wealth in farmland, and leads to insecurity of food. (â€Å"Water security†, 2010) Moreover, the amount of water needs for food production is the problem. People desire more and more water for even more agriculture.Yet the most major contributor to water scarcity and to the ecosystem is the way people use water (Molden, De Fraiture, & Rijisberman, 2007). In addition, the quantity, availability, and price of key food product inputs can be directly impacted upon by water scarcity having a negative affect on animal and crop yields. The price of food commodities is particularly vulnerable and defenseless to the shocks of unexpected extreme weather incidents, while animals yields are highly at risk from raised water temperatures especially aquaculture and access to clean water sources (Krechowicz, Venugopal, Sauer, Somani, & Pandey, 2010).Within the next ten to twenty years, the wate r crisis seems likely to trigger significant shortfalls in cereal production. As a result, an enormous global food crisis will occur (Quarterly, 2010). Water scarcity, the global critical issue cause increasing environmental stress, and it affects the ecosystem. In order to solve the water scarcity problem, huge dam construction causes interception of river flow, and it is endangering the dependent creatures.The study estimated 24% of mammals, 12% of birds, and 10% of freshwater fish types are endangered (â€Å"Water security†, 2010). Increasing consumption water not only decrease the amount of water for human development but has brought a profound influence on the aquatic ecosystems and their supported stocks (World Water Council, n. d. ). In addition, freshwater species also experience habitat degradation and changes of thermal regimes which relate to climate alteration and water impoundment (Arthurtonet al. , n. d. ).More than half of native freshwater in South Australia a re already listed as rare, endangered or vulnerable and the problem is worsening by the drought which makes conservation difficult, once their habitats dry up (â€Å"Water security†, 2010). Covich, Postel and Carpenter explain that the life those ecosystems support and the health of aquatic ecosystems are in the risk stage because of the withdrawal of more fresh water for industry, agriculture, or cities in many areas (as cited in Postel, 2000). Over and above, water scarcity brings a big effect on human health.The single most important issue determining public health which has been identified by the World Health Organization is clean water (â€Å"Problem: Fresh water†, n. d. ). The global water crisis causes death and disease in the world taking more than 14,000 people’s lives which include 11,000 of children under age five take each day (West, n. d. ). Poor water quality raises the risk of diarrhoeal diseases such as dysentery, typhoid fever, cholera, and othe r water-borne infections. Meantime, diseases such as trachoma, typhus, and plague are caused by water scarcity.People store water at home due to water shortage; this will increase the risk of household water contamination and providing mosquitoes with a breeding ground, which are carriers of malaria, dengue fever and other diseases (World Health Organization, n. d. ). Human health is the most important issue but now water crisis already put human health below the safety level. The ever-increasing world population is a prime cause of the water scarcity. As populations grow rapidly, industrial, agricultural and individual water demands increase (â€Å"Global water shortage†, n. . ). In the last century, global water consumption amplified six fold which is more than twice the speed of population increase and it is believed that water consumption will continue growing and outpace population growth in the future; however, the available freshwater is limited which is less than the one percent of the total water on the Earth (â€Å"Water scarcity and†, n. d. ). Postel predicted the world is now facing the issue of insufficient water supply and foresees that problem of water supply or water availability will get worse for the next 30years.Consequently, Sandra argued it raises the issues of water supply in agriculture, production for human demand due to increase of income, and providing drinking water (as cited in Environmentalist on Water Conservation, 2010). Water shortage also happens because of decreasing groundwater level. In 2000, global water withdrawal was predicted to be 30% of the world’s total available fresh water supply. Before 2025, this fraction might reach 70% (â€Å"Water security and†, 2010). The water level underground in different parts of the earth are called water tables (Edwin, 2010).Water tables are dropping because of the over-pumping out of groundwater in many countries in a large portion (â€Å"Problem: Fresh†, n. d. ) which already exceeds natural replenishment (â€Å"Water security and†, 2010). The lack of the rain water falling causes ground water to flow into the sea. This will cause a slow decrease of the ground water level and this has to be controlled to try to make the water table increase. Water mining is happening at  twice  the speed of natural renewal, causing aquifer water tables to fall by 3 to 10 feet per year in most parts of the country.As a result, the deeper the water table, the more tough it is for those who need to use it (Edwin, 2010). Water scarcity happens due to its distribution but not the total volume of water worldwide (King, 2010). There are various reasons which cause water shortage. Based on research, global warming is one of the major roots of water scarcity (â€Å"Problem: Fresh†, n. d. ). The global temperature rises which leads to upstream glaciers melting into water. This might possibly be permanent and will cause various rivers to reduce in size and some will disappear completely.As there is less snow and more rain, the sea water level increase will encroach into the lower reaches of the streams. There will be more flooding and runoff during the rainy season, but water held as ice and snow in the mountains will also be less for use in the dry season (King, 2010). Yet, global warming raises the chance of evaporation losses from the surfaces of rivers, lakes, and reservoir (Glennon. 2005). Climate change ‘contributes’ to the water deficiency. It brings intensive and more frequent droughts (â€Å"Water security and†, 2010).The sum of water available to refill groundwater sources impacted upon by the rate of evaporation differs a great deal, depending on relative humidity and temperature. Konikow and Kendy showed fleeting heavy rainfall and a fast evapotranspiration rate being combining together with high demand of water channels will cause groundwater reduction. Oki et al had explained that t he terrific temporal inconsistency in water resources worldwide leads to the unevenness of distribution of precipitation in space and time (Climate institute, n. . ). Severe floods inundate coast-lines to cause interruption of salt water into fresh water which is also brought by climate change. UN scientists calculate that climate change effect will probably account for about a fifth of the increase in water scarcity (â€Å"Water security and†, 2010). All told, water as a renewable source has faced crisis due to the several causes which are mentioned above. Government plays an important role in solving the water shortage problem.While the final  custodian of the national water resources must be the government and must play the key role in deciding strategies and frameworks (â€Å"Water†, n. d. ). Some governments instil some rules and regulations to ensure the water supply lasts longer, for example, Arizona’s Groundwater Management Act, which enforces regulati on on all users including cites, farms, and mines over 45years (Glennon, 2005). This innovative law results by starting an effective and comprehensive approach to groundwater management (Arizona Department of Water Resource, n. d. ).On the other hand, China’s 11th five year plan from year 2006 to 2010 is focused on the development of technological innovation and water works for ensuring water supply and the safety of drinking water; it is also improving flood control and mitigation of disaster, and enhancing water saving and conservation. In constructing water conservation programs, governments still have a critical task to play. (Glennon, 2005) An alternative solution for water shortage is implementing new multination water sharing treaties. Currently, there is a large quantity of treaties in effect concerning water, yet most of them do not distribute properly.These ineffective agreements will also lead to apprehension between nations. There are 261 major rivers’ wate rsheds presently shared by two or more nations (Gleick, n. d. ). The Rio Glande Compact which exits between the United States and Mexico has gone through debate, experiment and negotiation to reach agreement. Basically, a water sharing treaty distributes water based on land, population, and contribution to supply to ensure appropriate allocation. Reduced uncertainty or future population, industry and environmental needs are some of the benefits of the treaty (War, 2011).Furthermore, sharing a treaty can let both countries have the high cost-sharing; (Diar, 2008) yet can improve the economics of the country (War, 2011). To conclude this, a multinational treaty would be exceptionally beneficial in resolving water arguments as well as reducing animosity and tension between countries. As, 97. 5percent of water on the earth is seawater (Arthurtonet al. , n. d. ), desalination of seawater is one of the long term solutions for water scarcity (Medalla, 2009). Desalination means remove salt from seawater.Desalinisation is explained as filtering salty water through chemical membranes filters and removing the salt through electro dialysis and reverse osmosis leaving only fresh water as end product. In the Middle East and North Africa, about 130 nations have already worked by this procedure. However, the desalinization process has become much more practical for city areas and reverse-osmosis systems have attained significant enhancements recently. Arrandale shows globally implementing simple water recycling and filtration systems would be a relatively easy task that would reap outstanding benefits.Making these global advancements would be an economically viable and environmentally friendly sustainable green step in the right direction towards the reduction of global water scarcity (Schwikert, Hall, & Jen, n. d. ). If compared with ten years ago, the cost of desalination has considerably lowered; this shows that making this type of solution is now more practicable. The des alination industry has also undergone other positive developments and technological advancement in capacity and filtration that have reduced general operating costs (Medalla, 2009). In conclusion, the problem of water scarcity is growing.As more demand is made on limited supplies, the effort and cost to develop or even sustain access to water will rise (â€Å"Water scarcity: The†, n. d. ). Indeed, solution for water scarcity is a necessity which has been mentioned, such as water sharing treaties, environmentally opposed desalination solutions, and government’s rules, regulations and plans. Apart from corporation, agencies, and government’s efforts, everyone can contribute too. Every small thing makes a difference for the world. Furthermore, people can just buy only fair-trade products, only organics, only sustainably certified seafood, wood and paper (Caldecott, 2008).The next generations deserve a better future! References Arizona Department of Water Resource ( n. d. ). Securing Arizona’s water future. Retrieved from http://www. azwater. gov/AzDWR/WaterManagement/documents/Groundwater_Code. pdf Arthurton, R. , Barker, S. , Rast, W. , Huber, M. , Alder, J. , Chilton, J. , †¦ Wagne, G. (n. d. ). Water. Retrieved from http://www. unep. org/geo/geo4/report/04_water. pdf Caldecott, J. (2008). Water. The causes, costs and future of a global crisis. (2nd ed. ) London, Virgin Books. Climate institute. (n. d. ). Water. Retrieved from http://www. climate. org/topics/water. tml Dinar, S. (2008). Treaty principles and patterns: Negotiations over international rivers. Benefits and costs and/or under economic asymmetry. (6. 1. 2. 2. 4). Retrieved from http://books. google. com. my/books? id=zSvObjuN8wYC&pg=PA229&lpg=PA229&dq=benefits+of+%22Water+Sharing+Treaty%22+cost+sharing&source=bl&ots=_pdTyaOsbd&sig=0S7DAmeJ-c9f0hzkEDlu3aLdOUo&hl=en&ei=ZgyoTrCSLKje4QTOhvDcDw&sa=X&oi=book_result&ct=result&resnum=2&ved=0CCAQ6AEwAQ#v=onepage&q=benefits%20o f%20%22Water%20Sharing%20Treaty%22%20cost%20sharing&f=false Edwin, S. 2010). The various causes of water scarcity in the world. Retrieved from http://www. saching. com/Articles/The-Various-Causes-of-Water-Scarcity-in-the-World-254. html Environmentalist on Water Conservation. (2010). Retrieved from http://thegreatvixen. weebly. com/water-conservation. html FOA. (n. d. ) Water & poverty, an issue of life & livelihoods. Retrieved from http://www. fao. org/nr/water/issues/scarcity. html Frank A. Ward. (2011). Presentation from the 2011World Water Week in Stockholm [Power Point slides]. Retrieved from http://www. worldwaterweek. rg/documents/WWW_PDF/2011/Monday/K24/Hydroeconomic-Modelling-in-Basins/Hydroeconomic-Modeling-in-Basins-Practice-Challenges-and-Reward. pdf Geoffrey, L. (2009). Water scarcity now bigger threat than financial crisis. Retrieved from http://www. independent. co. uk/environment/climate-change/water-scarcity-now-bigger-threat-than-financial-crisis-1645358. html Glei ck, P. H. (n. d. ). Making every drop count. Retrieved from http://web. macam. ac. il/~arnon/Int-ME/water/MAKING%20EVERY%20DROP%20COUNT. htm Global Water Shortage Looms In New Century (n. d. ). Retrieved from http://ag. arizona. edu/AZWATER/awr/dec99/Feature2. tm King, B. (2010). Scarcity of water. Retrieved from http://www. greeniacs. com/GreeniacsArticles/Water/Scarcity-of-Water. html Krechowicz, D. ,Venugopal, S. , Sauer, A. , Somani, S. , & Pandey, S. (2010). Weeding Risk: Financial Impacts of Climate Change and Water Scarcity on Asia’s Food and Beverage Sector. Retrieved from http://www. wri. org/publication/weeding-risk-asia Medalla, E. (2009). Hatch: Desalination is the solution for water scarcity in the north. Retrieved from http://www. bnamericas. com/news/waterandwaste/Hatch:_Desalination_is_the_solution_for_water_scarcity_in_the_north

Facilitation of Conditioned Fear Extinction

Neuroscience 134 (2005) 247–260 FACILITATION OF CONDITIONED FEAR EXTINCTION BY D-CYCLOSERINE IS MEDIATED BY MITOGEN-ACTIVATED PROTEIN KINASE AND PHOSPHATIDYLINOSITOL 3-KINASE CASCADES AND REQUIRES DE NOVO PROTEIN SYNTHESIS IN BASOLATERAL NUCLEUS OF AMYGDALA Y. L. YANGa AND K. T. LUb* Institute of Biotechnology, Department of Molecular Biology and Biochemistry, National Chia-Yi University, 300 University Road, Chia-Yi, Taiwan b Department of Life Science, National Taiwan Normal University, 88 Ming-Chow Road, Sec 4, Taipei, Taiwan aKey words: extinction, D-cycloserine, MAPK, PI-3 kinase, amygdala. Abstract—Recent results showed that either systemic or intra-amygdala administration of D-cycloserine, a partial agonist at the glycine modulatory site on the glutamate N-methylD-aspartate receptor facilitates the extinction of conditioned fear. Here we evaluated the role of mitogen-activated protein kinase and phosphatidylinositol 3-kinase in the basolateral nucleus of amygdala on the effect of D-cycloserine.The facilitation effect of D-cycloserine on fear extinction and mitogen-activated protein kinase activation was completely blocked by intra-amygdala administration of mitogen-activated protein kinase inhibitor PD98059 (500 ng/side, bilaterally) or U0-126 (20 M/side, bilaterally). Furthermore, phosphatidylinositol 3-kinase inhibitor (wortmannin, 5. 0 g/side, bilaterally) infused into the basolateral nucleus of amygdala signi? cantly reduced both facilitation effect of D-cycloserine and phosphatidylinositol 3-kinase activation.Intra-amygdala administration of a transcription inhibitor (actinomycin D, 10 g dissolved in 1. 6 l vehicle; 0. 8 l per side) and a translation inhibitor (anisomycin, 125 g dissolved in 1. 6 l vehicle; 0. 8 l per side) completely blocked the facilitation effect of D-cycloserine. Control experiments indicated the blockage by actinomycin D or anisomycin were not due to lasting damage to the basolateral nucleus of amygdala or state d ependency. In addition, none of the active drugs used here altered the expression of conditioned fear.These results suggested that phosphatidylinositol 3-kinase and mitogenactivated protein kinase-dependent signaling cascades and new protein synthesis within the basolateral nucleus of amygdala played important roles in the D-cycloserine facilitation of the extinction of conditioned fear.  © 2005 Published by Elsevier Ltd on behalf of IBRO. *Corresponding author. Tel: 886-2-29333149Ãâ€"234; fax: 886-229312904. E-mail address: [email  protected] ntnu. edu. tw (K. -T. Lu).Abbreviations: ACT DCS, actinomycin D D-cycloserine; ACT SAL, actinomycin D saline; ANI DCS, anisomycin D-cycloserine; ANI SAL, anisomycin saline; BLA, basolateral nucleus of the amygdala; CS, conditioned stimulus; DCS, D-cycloserine; EDTA, ethylenediaminetetraacetic acid; ISI, interstimulus interval; MAPK, mitogen-activated protein kinase; NMDA, N-methyl-D-aspartate; PD DCS, PD98059 D-cycloserine; PD SAL, PD9805 9 saline; PI-3K, phosphatidylinositol 3-kinase; US, unconditioned stimulus; U0 DCS, U0-126 D-cycloserine; U0 SAL, U0126 saline; VEH DCS, vehicle D-cycloserine; VEH SAL, vehicle saline; WH DCS, wortmannin D-cycloserine; WH SAL, wortmannin saline. 0306-4522/05$30. 00 0. 00  © 2005 Published by Elsevier Ltd on behalf of IBRO. doi:10. 1016/j. neuroscience. 2005. 04. 003 Fear conditioning occurs when a previously neutral stimulus (conditioned stimulus) is paired with an aversive stimulus (McAllister and McAllister, 1971).Following such pairing the conditioned stimulus is thought to elicit a state of conditioned fear. This is de? ned in animals by their behavior: freezing, autonomic reactivity, and fear-potentiated startle. A large literature indicates that the basolateral nucleus of the amygdala (BLA) is critically involved in both the acquisition and the expression of conditioned fear (Davis, 2000). Neurotoxic lesions or intra-amygdala infusion of glutamate antagonists into the BLA bl ocks the expression of conditioned fear. In addition, local infusion of N-methyl-D-aspartate (NMDA) speci? c antagonists blocks the acquisition of conditioned fear (Miserendino et al. , 1990; Kim et al. , 1991; Maren et al. , 1996; Gewirtz and Davis, 1997).Synaptic plasticity in this area is thought to underlie the learning process when afferent sensory information elicited by the conditioned stimulus is paired with afferent pain information elicited by the unconditioned stimulus (Fanselow and LeDoux, 1999). Extinction is de? ned as a reduction in conditioned fear when the conditioned stimulus (CS) is presented repeatedly in the absence of the unconditioned stimulus (US). Many studies show that extinction is not the result of forgetting or memory erasure but results from formation of new associations that compete with prior fear-conditioned associations (Falls and Davis, 1995; Davis et al. , 2000). Similar to acquisition, extinction is also blocked by glutamate NMDA receptor antagon ists either given systemically (Cox and Westbrook, 1994; Baker and Azorlosa, 1996; Kehoe et al. 1996) or locally infused into the BLA (Falls and Davis, 1992). The glycine modulatory site of the NMDA receptor provides a critical regulatory role. Whereas direct NMDA agonists may be neurotoxic due to unregulated calcium entry, partial agonists can facilitate glutamatergic NMDA activity in a more limited fashion (Lawler and Davis, 1992; Olney, 1994). Recent results showed that partial agonists acting at the glycine modulatory site of the NMDA receptor, such as D-cycloserine (DCS), enhance learning and memory in several animal models (Thompson and Disterhoft, 1997; Pussinen et al. , 1997; Matsuoka and Aigner, 1996; Land and Riccio, 1999; Walker et al. , 2002; 247 248 Y. L. Yang and K. T.Lu / Neuroscience 134 (2005) 247–260 extinction test, an extinction training and a post-extinction test (see Fig. 1A). Acclimation. On each of 3 consecutive days, rats were placed in the test chamb ers for 10 min and then returned to their home cages. Baseline startle test. On each of the next 2 consecutive days, animals were placed in the test chambers and presented with 30 95-dB startle stimuli at a 30-s interstimulus interval (ISI). Animals whose baseline startle response was 1% of the measurable level were not included in later analysis. Fear conditioning. Twenty-four hours later, rats were returned to the test chambers and after 5 min were given the ? rst of 10 light-footshock pairings.The shock (US) was delivered during the last 0. 5 s of the 3. 7 s light (CS). The average intertrial interval was 4 min (range 3–5 min) and the shock intensity was 0. 6 mA. Pre-extinction test. Twenty-four hours after fear conditioning, rats were returned to the test chambers and 5 min later presented with 30 startle-eliciting noise bursts (95 dB, 30 s ISI). These initial startle stimuli were used to habituate the startle response to a stable baseline prior to the light-noise test tr ials that followed. Thirty seconds later a total of 20 startle-eliciting noise bursts were presented, 10 in darkness (noise alone) and 10 3. 2 s after onset of the 3. s light (light-noise) in a balanced, irregular order at a 30-s ISI. Percent fear-potentiated startle was computed as [(startle amplitude on light-noise noise-alone trials)/noisealone trials] 100. Rats were then divided into equal size groups of comparable mean levels of percent fear-potentiated startle. Rats with less than 50% fear-potentiated startle during the pre-extinction test were not used. Extinction training. Extinction training (cue exposure) is de? ned as the repetitive exposure to the CS cue (light) in the absence of the US (shock). Twenty-four hours after the preextinction test, rats were returned to the test chamber. After 5 min, they were presented with 30, 3. s light exposures at a 30-s ISI. Context control groups (context exposure) remained in the test cages for the same amount of time but did not recei ve light presentations. Extinction training was performed for varying numbers of consecutive days (2 days for experiment 1 and 1 day for subsequent experiments). Post-extinction test-1. Twenty-four hours after the last extinction training, rats were returned to the test chamber. After 5 min, they were presented with 30 95-dB leader stimuli for a habituated startle baseline. This was followed by a total of 60 startle-eliciting noise bursts, 30 in darkness (noise alone) and 30 presented 3. 2 s after onset of the 3. s light (light-noise) in a balanced, irregular order at a 30-s ISI. Results were evaluated the same way as pre-extinction test. Post-extinction test-2. Twenty-four hours after the extend extinction training period, rats were returned to the test chamber and process the post-extinction test described above. Fear-potentiated startle test. Twenty-four hours after fear conditioning, rats were returned to the test chamber and testing for fear-potentiated startle using the post-e xtinction test-1 described above. Ledgerwood et al. , 2003; Richardson et al. , 2004). In addition, ( )-HA966, a competitive antagonist at the glycine regulatory site on the NMDA receptor, reversed the DCS effect (Walker et al. , 2002).Clinical studies have shown that DCS can sometimes enhance implicit memory and improve cognition in patients with Alzheimer’s disease (Schwartz et al. , 1996; Tsai et al. , 1998, 1999). It can also counter cognitive de? cits in schizophrenia (Javitt et al. , 1994; Goff et al. , 1999). Furthermore, systemic administration of DCS also proved to facilitate extinction of conditioned fear (Walker et al. , 2002; Ledgerwood et al. , 2003, 2004; Ressler et al. , 2004). Numerous signaling cascades including mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI-3K) and calcineurin, are involved in the extinction of conditioned fear (Lu et al. , 2001; Lin et al. , 2003).Similar mechanisms may also be involved in the facilitation effec t of DCS. This study was designed to clarify the relationship between amygdaloid NMDA receptors, MAPK and PI-3K signal cascades on the extinction of conditioned fear. EXPERIMENTAL PROCEDURES Animals Adult male Sprague–Dawley (SD) rats (obtained from the animal center of National Taiwan University Taipei, Taiwan) weighing between 250 and 350 g were used. Animals were housed in groups of four rats in a temperature (24  °C) -controlled animal colony with continuous access to food and water. Rats were kept on a 12-h light/dark cycle with lights on at 07:00 h. All behavioral procedures took place during the light cycle.All procedures were conducted in accordance with the National Institutes of Health Guide for Care and Use of Laboratory Animals and the guidelines set forth by the Institutional Animal Care and Use Committee at the National Taiwan Normal University. In all experimental procedures involving animals, all efforts were made to minimize pain and the number of animals u sed. Surgery All surgeries were carried out under sodium pentobarbital (50 mg/ kg, i. p. ) anesthesia. Once anesthetized, the rat was placed in a Kopf stereotaxic instrument, the skull was exposed, and 22 gauge guide cannula (model C313G, Plastic-one Products, Roanoke, VA, USA) were implanted bilaterally into the BLA (AP, 2. ; DV, 9. 0, ML, 5. 0 from bregma (Paxinos and Watson, 1997)). Size 0 insect pins (Carolina Biological Supply, Burlington, NC, USA) were inserted into each cannula to prevent clogging. These extended about 2 mm past the end of the guide cannula. Screws were anchored to the skull and the assembly was cemented in place using dental cement (Plastic-one Products). Rats received an antibiotic (penicillin) once every day for the ? rst 3 days after the surgery to reduce the risk of infection. General behavioral procedures Fear conditioning was measured using the potentiated startle paradigm (Cassella and Davis, 1986; Lu et al. , 2001; Walker et al. , 2002).The rats were trained and tested in a startle chamber (San Diego Instruments, San Diego, CA, USA) in which cage movement resulted in the displacement of an accelerometer. Startle amplitude was de? ned as peak accelerometer voltage within 200 ms after startle stimulus onset. The behavioral procedures common to all experiments consisted of an acclimation phase, a baseline startle test phase, a fear conditioning phase, a pre- Drug injection DCS (Sigma) was freshly dissolved in saline. DCS (15 mg/kg, i. p. ) or saline was injected intraperitoneally 15 min prior to extinction training with a 26 gauge injection needle connected to a 1 ml syringe (Walker et al. , 2002; Ledgerwood et al. , 2003) (experiments 1– 8).MAPK inhibitor PD98059 (500 ng in 1 l of 20% DMSO; Calbiochem) (Lu et al. , 2001) or U0-126 (50 ng/side; Sigma) (Lin et al. , 2003) or 20% DMSO was infused into the BLA Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 249 Fig. 1. Systemic administration of DCS accelerate d extinction of conditioned fear. (A) Timeline of behavioral procedures for experiment 1. (B) Percent fear-potentiated startle measured 24 h before (pre-extinction test) and 24 h after extinction training (post-extinction test). Rats in each group were treated with either DCS or saline prior to a single session of extinction training. (C) To test for toxicity, after 24 h all animals of experiment 1 were retrained.They were tested for fear-potentiated startle response in the absence of drugs 24 h later (fear-potentiated startle test) (values are mean SEM, * P 0. 05 versus control group; # P 0. 05 versus the group with 1 day extinction and saline injection). 250 Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 10 min prior to saline or DCS injection (experiments 2 and 8). PI-3K inhibitor (wortmannin, 5 g/side) (Lin et al. , 2003) or vehicle was administrated to the BLA 10 min prior to saline or DCS injection (experiment 3). Transcription inhibitor actinomycin D (10 g d issolved in 1. 6 l vehicle; 0. 8 l per side) or translation inhibitor (anisomycin, 125 g dissolved in 1. 6 l vehicle; 0. 8 l per side) or vehicle (Lin et al. 2003) was administrated to the BLA 10 min prior to DCS or saline injection (experiment 4) or 25 min prior to fear-potentiated startle test (experiment 6). In the control experiment, PD98059, U0-126, wortmannin, actinomycin D, and anisomycin were injected 25 min prior to the fear-potentiated startle test. Injections were made through 28-gauge injection cannula (model C313I, Plastic-one Products) connected to a Hamilton micro-syringe via polyethylene tubing. Infusion speed was 0. 25 l/ min. The total volume of injection was 0. 8 l per side. Western blot analysis Animals were killed by decapitation 10 min after extinction training. The lateral and basolateral subregions of the amygdala were collected and sonicated brie? y in ice-cold buffer: 50 mM Tris–HCl (pH 7. ), 50 mM NaCl, 10 mM EGTA, 5 mM EDTA, 2 mM sodium pyrophospha te, 4 mM para-nitrophenylphosphate, 1 mM sodium orthovanadate, 1 mM phenylmethylsulfonyl ? uoride (PMSF), 20 ng/ml leupeptin, and 4 ng/ml aprotinin. Following sonication, the soluble extract was obtained after pelleting the crude membrane fraction in a centrifuge at 50,000 g at 4  °C. Protein concentration in the soluble fraction was then measured using a Bradford assay with bovine serum albumin as the standard. Equivalent amounts of protein for each sample were resolved in 10% sodium dodecyl sulfate (SDS)–polyacrylamide gels, blotted electrophoretically to PVDF membranes and blocked overnight in 5% skim milk (Cell Signaling Technology, Inc. , USA).Blots were incubated with antiphospho-ERK antibody (New England Biolabs, USA), anti-ERK antibody (BD Transduction Laboratories, USA), anti-phospho-Akt antibody (New England Biolabs) or anti-pan-Akt (BD Transduction Laboratories). Band detection was performed with an enhanced chemiluminescence Western blotting analysis system (RPN 2108; Amersham International, Amersham, UK). fear-potentiated startle during the pre-extinction test. The ? nal 30 rats were assigned into ? ve groups of six animals based on their level of fear-potentiated startle in the preextinction test. Twenty-four hours after the pre-extinction test, each rat received 1 or 2 consecutive days of extinction training with DCS (15 mg/kg, i. p. ) or saline. Saline or DCS was injected 15 min prior to the extinction training.An additional control group was tested 2 days after the pre-extinction training without intervening exposures to visual CS. Fig. 1B shows that DCS accelerated extinction of conditioned fear. A two way ANOVA for differences in treatment (DCS vs saline) and days (one or two extinction sessions) between-subjects indicated a signi? cant treatment effect (F(1,20) 9. 02) and a signi? cant treatment days interaction (F(2,20) 6. 68). Thus, the reduction of fear-potentiated startle after 1 day of extinction training was greater in the gr oup that received DCS than in the group that received saline (Fig. 1B). Individual comparisons between DCS- and saline-treated groups indicated signi? ant differences after 1 day of extinction sessions (t(10) 3. 86). Previous studies have shown that lesions of the BLA block expression of fear-potentiated startle (Campeau and Davis, 1995). DCS may have toxic effect on BLA, and resulting misinterpretation of its facilitation effects on extinction. To test for toxicity, all animals of experiment 1 were retrained and tested 24 h later. Under these conditions, animals previously injected with DCS or saline showed a signi? cant fear-potentiated startle (Fig. 1C). Thus, the facilitation effect of DCS observed during the post-extinction test 1 appeared to result from the acute drug effect rather than from a more permanent, perhaps toxic, action of DCS.Experiment 2: intra-amygdala infusion of MAPK inhibitors blocked the facilitation of extinction by DCS To test the possible role of MAPK-depe ndent signaling cascade in the DCS-enhanced effect on the extinction of condition fear, 48 rats received fear conditioning, extinction training, and testing for fear-potentiated startle. Initially, 58 rats were used, but 10 of them were excluded. Rats were randomly assigned to six different groups and received one of the following treatments: vehicle saline (VEH SAL), vehicle DCS (VEH DCS), PD98059 DCS (PD DCS), U0-126 DCS (U0 DCS), PD98059 saline (PD SAL) or U0-126 saline (U0 SAL). The MAPK inhibitors, PD98059, and U0-126 (or vehicle) were administrated to the BLA 10 min prior to the injection with DCS or saline. Animals were then returned to their cage.Fifteen minutes after injection, animals were subjected to a single session of extinction training. Previously, we show that a single day of extinction training with cue exposure led to about 35% decrease in fear-potentiated startle, whereas 2–3 days of extinction training led to near complete extinction (Lu et al. , 2001; Wa lker et al. , 2002). We concluded that the acceleration of extinction is best detected after a single session of extinction training. As shown in Fig. 2, DMSO, PD98059 (500 ng/side, bilaterally), or U0-126 (20 nM/per side, bilaterally) was given 10 min prior to saline or DCS injection; rats were returned to their cages for 30 min before a single HistologyRats were overdosed with chloral hydrate and perfused intracardially with 0. 9% saline followed by 10% formalin. The brains were removed and immersed in a 30% sucrose-formalin solution for at least 3 day. Coronal sections (30 M) were cut through the area of interest, stained with Cresyl Violet, and examined under light microscope for cannula placement. Animals with misplaced cannula were not included in later analysis. Statistical analysis The mean startle amplitude across the 30 noise alone and 30 light-noise trials during the pre- and post-extinction tests was calculated for each animal. All results were analyzed using a score of percent fear-potentiated startle, as de? ned in the post-extinction tests above.ANOVA on scores was the primary statistical measure. Between-group comparisons were made using two-tailed t-tests for independent samples. The criterion for signi? cance for all comparisons was P 0. 05. RESULTS Experiment 1: systemic administration of DCS accelerated extinction of conditioned fear This experiment assessed the facilitation effect of DCS on different amounts of extinction training. Initially, 35 rats were used. Five were excluded for showing less than 50% Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 251 Fig. 2. Intra-amygdala infusion of MAPK inhibitors blocked facilitation effect of DCS on extinction. (A) Timeline of behavioral procedures for experiment 2. B) Cannula was placed in the BLA. Percent fear-potentiated startle measured 24 h before (pre-extinction test) and 24 h after extinction training (post-extinction test). Rats in each group underwent VEH SAL, VEH DCS, PD DCS, U0 DCS, PD SAL, or U0 SAL prior to a single session of extinction training. Twenty-four hours later, animals were tested for fear-potentiated startle in the absence of drugs (values are mean SEM, * P 0. 05 versus VEH SAL group; # P 0. 05 versus VEH DCS group). (C) Cannula tip placements transcribed onto atlas plates adapted from Paxinos and Watson (1997). 252 Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 session of extinction training.Twenty-four hours later, animals were tested for fear-potentiated startle in the absence of drugs. Results showed that there was a signi? cant overall difference between treatments (F(5,42) 11. 81). Fig. 2 shows that administration of DCS facilitated extinction of conditioned fear (VEH DCS) compared with the control group (VEH SAL) (t(14) 3. 12, P 0. 05). This effect was blocked by co-administration of MAPK inhibitor PD98059 (PD DCS) or U0-126 (U0 DCS) (t(14) 3. 08, P 0. 05 and t(14) 3. 29, P 0. 05, respectively) compared wit h the control (VEH DCS), treated with PD98059 only (PD SAL) or U0-126 only (U0 SAL) did not affect extinction (t(14) 0. 7 and t(14) 0. 36, respectively). These results indicated that the MAPK dependent signaling cascade most likely mediated the facilitation effect of DCS. Experiment 3: intra-amygdala infusion of the PI-3K inhibitor blocked facilitation of extinction by DCS Previous ? ndings have shown that PI-3K inhibitors retard acquisition in a variety of learning paradigms (Lin et al. , 2003). To evaluate the possible role of PI-3K signaling cascade in the DCS enhancement of extinction of conditioned fear, 32 rats received fear conditioning, extinction training, and testing for fear-potentiated startle. Although 38 rats were used initially, six were excluded.They were then randomly assigned to four different groups and received one of the following treatments: VEH SAL, VEH DCS, wortmannin DCS (WH DCS) and wortmannin saline (WH SAL). The PI-3K inhibitor (wortmannin, 5 g/side, bila terally) was infused to the BLA 10 min prior to the injection of saline or DCS. Then rats were returned to their cages for 15 min before being subjected to a single session of extinction training. Twenty-four hours later, animals were tested for fear-potentiated startle in the absence of drugs. Results showed that there was a signi? cant overall difference between treatments (F(4,28) 12. 17). As shown in Fig. 3, the facilitation effect of DCS (VEH DCS) on extinction was blocked by co-administration of PI-3K inhibitor (WH DCS) (t(14) 2. 98, P 0. 05).With the single extinction training session used in this experiment, this dose of wortmannin alone (WH SAL) at this dose had no effect on the extinction of fear-potentiated startle compared with control group (VEH SAL) (t(14) 0. 19). These results suggest that the PI-3K signaling cascade was involved in the DCS facilitation of extinction. Experiment 4: DCS enhanced the extinction training induced MAPK and PI-3K phosphorylation According t o the results of the above experiments, the DCS facilitation effect on extinction was prevented by coadministration of MAPK or PI-3K inhibitor. Previous studies have shown that infusion of these same inhibitors blocks extinction (Lu et al. , 2001; Lin et al. , 2003). Therefore, these treatments in conjunction with DCS must result in no extinction and resulting misinterpretation of its blockage effects on DCS.To show the MAPK and PI-3K signaling pathways are essential for the facilitation effect of DCS, we used Western blot to evaluate the DCS effect on the extinction training induced MAPK and PI-3K phosphorylation. Additional amygdala-cannulated rats received fear conditioning, extinction training, and testing for fear-potentiated startle. Then PD98059 or wortmannin was infused to the BLA 10 min prior to the injection of saline or DCS. Rats were returned to their cages. Fifteen minutes after DCS or saline injection, animals were subjected to a single session of extinction training. Animals were killed by decapitation 10 min after extinction training.The lateral and basolateral sub-regions of the amygdala were tested with Western blot analysis. Compared with control group, MAPK phosphorylation was signi? cantly elevated in BLA after extinction training (Fig. 4A, lane 2). Administration of DCS enhanced the effect of extinction training on MAPK phosphorylation (Fig. 4A, lane 3). The MAPK inhibitor PD98059 blocked the effect of DCS (Fig. 4A, lane 4). In addition, we measured the state of Akt phosphorylation as an index of PI-3K activity (Lin et al. , 2001). Fig. 4B showed that administration of DCS enhanced the effect of extinction training on Akt phosphorylation (Fig. 4B, lane 3). The PI-3K inhibitor, wortmannin, blocked the enhancement effect of DCS (Fig. 4b, lane 4).These results raise the possibility that DCS enhancement effect of extinction of conditioned fear is mediated by the amygdaloid MAPK and PI-3K dependent signaling cascades. Experiment 5: intra-amygd ala infusion of the transcription inhibitor or translation inhibitor blocked DCS facilitation of extinction The MAPK pathway participates in the synthesis of proteins important for the long-term stabilization and storage of fear memories. According to the result of experiment 2, the facilitation effect of DCS on extinction is mediated by the MAPK dependent signaling cascade. We predicted that the facilitation effect of DCS required new protein synthesis in the BLA.To test this hypothesis, 48 rats received fear conditioning, extinction training, and testing for fear-potentiated startle. Initially, 56 rats were used but eight of them were excluded. Rats were then randomly assigned to six different groups and received one of the following treatments: VEH SAL, VEH DCS, actinomycin D DCS (ACT DCS), anisomycin DCS (ANI DCS), actinomycin D saline (ACT SAL), and anisomycin saline (ANI SAL). Transcription inhibitor (actinomycin D, 10 g dissolved in 1. 6 l vehicle; 0. 8 l per side) and transl ation inhibitor (anisomycin, 125 g dissolved in 1. 6 l vehicle; 0. 8 l per side) were administered to the BLA 10 min prior to saline or DCS injection. Then rats were returned to their cages. Fifteen minutes later, nimals were subjected to a single session of extinction training. Twenty-four hours later, animals were tested for fear-potentiated startle in the absence of drugs. Results showed that there was a significant overall difference between treatments (F(5,42) 10. 17). As shown in Fig. 5, actinomycin D and anisomycin completely blocked the facilitation effect of DCS (t(14) 3. 11 and t(14) 2. 96, respectively) compared with the VEH DCS group. With a single extinction training session used in this experiment, actinomycin alone (ACT SAL) or anisomycin alone (ANI SAL) did not affect the extinction of fear-potentiated startle compared with control Y. L. Yang and K. T.Lu / Neuroscience 134 (2005) 247–260 253 Fig. 3. Intra-amygdala infusion of the PI-3K inhibitor blocked the fa cilitation effect of DCS on extinction. (A) Timeline of behavioral procedures for experiment 3. (B) Cannula was placed in the BLA. Percent fear-potentiated startle measured 24 h before (pre-extinction test) and 24 h after (post-extinction test) extinction training. Rats in each group were treated with VEH SAL, VEH DCS, WH DCS, or WH SAL prior to a single session of extinction training. Twenty-four hours later, animals were tested for fear-potentiated startle in the absence of drugs (values are mean SEM, * P 0. 05 versus VEH SAL group). C) Cannula tip placements transcribed onto atlas plates adapted from Paxinos and Watson (1997). 254 Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 (VEH SAL) (t(14) 0. 88 and t(14) 0. 48, respectively). These results suggest that new protein synthesis within the BLA played an important role in DCS facilitation of extinction of conditioned fear. Experiment 6: the disruptive effect of intra-amygdala infusion of actinomycin D and anisomy cin was not attributed to lasting damage to the amygdala The active drugs used in the above experiments may have toxic effect within the amygdala. Previous work shows that infusion of PD98095 (Lu et al. , 2001) or wortmannin (Lin et al. 2003) into BLA did not appear to cause permanent impairment of amygdala function. To test for possible toxic effects of actinomycin D and anisomycin on the BLA, all animals of experiment 5 received an additional 2 days of drug free extinction training followed 24 h later by testing. Under these conditions, rats previously treated with actinomycin D (ACT DCS-treated group and ACT SALtreated group) or anisomycin (ANI DCS- and ANI SALtreated group) showed a signi? cant reduction of fearpotentiated startle between post-extinction test 1 and post-extinction test 2 (t(7) 3. 08 and t(7) 3. 32 for the ACT DCS-treated group and ACT SAL-treated group respectively) and (t(7) 2. 96 and t(7) 3. 1 for the ANI DCStreated group and ANI SAL-treated group respectively ) (Fig. 6B). Thus, the blockage of extinction observed during post-extinction test 1 appeared to result from an acute drug effect rather than from a more permanent and perhaps toxic action, of actinomycin D or anisomycin. Previous studies have shown that lesions of the BLA block fear-potentiated startle (Campeau and Davis, 1995), an outcome opposite from that obtained with infusion of actinomycin D or anisomycin. It is also important to note that actinomycin D or anisomycin may have long-term toxicity within the BLA. The extinction of fear would look the same as a gradual loss of ability to express or relearn fear.Experiment 7: the disruptive effect of intra-amygdala infusion of actinomycin D and anisomycin was not attributed to state dependency To evaluate the contribution of state-dependency effects to the results obtained in experiment 6, additional amygdala-cannulated rats were tested for extinction in a drug-free state and after receiving the same compound that they had receive d during extinction training. Results showed that there was a signi? cant overall difference between treatments in post-extinction test 2 (F(2,21) 32. 16). These results are shown in Fig. 7. Rats infused with actinomycin or anisomycin before postextinction test 2 showed a slight, but non-signi? cant, decrease in fear-potentiated startle from post-extinction test 1 to post-extinction test 2. For control rats (n 8), fear-potentiated startle was signi? cantly lower during post-extinction test 2 than post-extinction test 1 (t(7) 2. 455; P 0. 05). The lost of fear-potentiated startle in both groups probably re? cted incidental extinction produced by the 30 non-reinforced CS presentations of post-extinction test 1. The failure of rats infused before Fig. 4. MAPK and PI-3K inhibitors blocked extinction training activation of MAPK and PI-3K. (A) Representative Western blots and densitometric analysis of the activation of MAPK in the BLA under different treatments (values are mean SEM, * P 0 . 05 versus VEH SAL group). (B) Representative Western blots and densitometric analysis Akt phosphorylation as an index of PI-3K activity in the BLA under different treatments (values are mean SEM, * P 0. 05 versus VEH DCS group). Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 255 Fig. 5.Intra-amygdala infusion of the transcription inhibitor or translation inhibitor blocks the facilitation effect of DCS on extinction of conditioned fear. (A) Timeline of behavioral procedures for experiment 5. (B) Cannula was placed in the BLA. Percent fear-potentiated startle measured 24 h before (pre-extinction test) and 24 h after (post-extinction test 1) extinction training. Rats underwent treatment with VEH SAL, VEH DCS, ACT DCS, ANI DCS, ACT SAL, or ANI SAL prior to a single session of extinction training. Twenty-four hours later, animals were tested for fear-potentiated startle in the absence of drugs (values are mean SEM, * P 0. 05 comparing with the VEH SAL group; # P 0. 05 compared with the VEH DCS group). C) Cannula tip placements transcribed onto atlas plates adapted from Paxinos and Watson (1997). 256 Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 Fig. 6. The disruptive effects of intra-amygdala infusion of actinomycin D and anisomycin on extinction were not attributed to lasting damage to the BLA. (A) Timeline of behavioral procedures for experiment 6. The same animals used in experiment 3 were subjected for two more trials of extinction training. (B) Twenty-four hours after the last extinction training, animals were tested for fear-potentiated startle in the absence of drugs (post-extinction test-2) (values are mean SEM, * P 0. 05 versus the corresponding post-extinction test-2). esting with the transcription and translation inhibitors before testing to show a loss of fear-incidental extinction suggested that state dependency was not a major factor in the effects of actinomycin D and anisomycin. Experiment 8: effect of pretest PD98059, U0-126, wortmannin, actinomycin, and anisomycin administration on fear-potentiated startle This experiment was designed to evaluate whether the effect of the active drugs used has had a secondary effect on fear itself or on CS processing. For example, if MAPK inhibitor U0-126 reduced CS-elicited fear, this might attenuate extinction by decreasing the discrepancy between CS predictions and what actually occurred. If actinomycin D or anisomycin interfered with visual processing, this might block extinction produced by non-reinforced exposures to the visual CS.To evaluate these possibilities, 42 amygdala-cannulated rats received acclimation, baseline startle test, and fear conditioning. Initially, 50 rats were used, but eight of them were excluded. After 24 h, rats were infused with PD98059, U0-126, wortmannin, actinomycin, and anisomycin. At 25 min after the infusions, rats were tested for fear-potentiated startle. As shown in Fig. 8, none of the active drugs we used here sig ni? cantly in? uenced fearpotentiated startle (F(6,35) 0. 993). Thus, it is unlikely that these drugs in? uenced extinction by increasing fear or by disrupting CS processing. Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 57 Fig. 7. The disruptive effect of intra-amygdala infusion of actinomycin D and anisomycin were not attributed to state dependency. (A) Timeline of behavioral procedures for experiment 7. (B) Cannula was placed in the BLA. Percent fear-potentiated startle measured 24 h before (pre-extinction test), 24 h after (post-extinction test 1), and 48 h after (post-extinction test 2) extinction training. Rats in each group underwent VEH SAL, ACT DCS, or ANI DCS prior to a single session of extinction training and prior to post-extinction test 2. Animals were tested for fear-potentiated startle in the absence of drugs (values are mean SEM, * P 0. 05). C) Cannula tip placements transcribed onto atlas plates adapted from Paxinos and Watson (1997). 258 Y. L. Y ang and K. T. Lu / Neuroscience 134 (2005) 247–260 Fig. 8. Effect of pretest PD98059, U0-126, wortmannin, actinomycin, and anisomycin administration on fear-potentiated startle. (A) Timeline of behavioral procedures for experiment 8. (B) Cannula was placed in the BLA. Percent fear-potentiated startle was measured 24 h after fear conditioning. Rats were treated with DMSO, PD98059 (PD), U0-126 (U0), wortmannin (WH), vehicle (VEH), actinomycin (ACT), or anisomycin (ANI) 25 min prior to the fear-potentiated startle test (values are mean SEM). C) Cannula tip placements transcribed onto atlas plates adapted from Paxinos and Watson (1997). DISCUSSION We build on the previous ? ndings that DCS facilitated extinction of conditioned fear (Walker et al. , 2002; Ledgerwood et al. , 2003, 2004; Ressler et al. , 2004). Here, we show for the ? rst time that the DCS effect was prevented by co-administration of MAPK, PI-3K, transcription, and translation inhibitors. Control experiments indica ted that the blocking effects of actinomycin D and anisomycin on extinction were not due to lasting damage to the BLA or state dependency. In addition, none of active drugs we used in this study altered the expression of conditioned fear.These results suggest that PI-3K and MAPK-dependent signaling cascades and de novo protein synthesis within the BLA were important for DCS facilitation. Early behavioral studies by Pavlov (1927) and Konorski (1948) de? ned extinction as an active process involving formation of new inhibitory associations as opposed to forgetting previously conditioned associations. Numerous studies since have con? rmed and elaborated these early ? ndings (reviewed in Falls and Davis, 1995; Davis et al. , 2000). It is now well accepted that extinction occurs with repeated presentation of a CS in the absence of the pre- Y. L. Yang and K. T. Lu / Neuroscience 134 (2005) 247–260 259 viously paired US.This reduces the conditioned response elicited by the CS. In co ntrast to forgetting which implies the passive loss of memory, extinction implies active formation of new inhibitory associations competing with and overpowering original excitatory associations. Evidence is growing that extinction may involve circuits and use mechanisms of synaptic plasticity similar to those of conditioned fear learning (Falls and Davis, 1992; Cox and Westbrook, 1994; Baker and Azorlosa, 1996; Davis et al. , 2000). NMDA-dependent synaptic plasticity appears to mediate many forms of active learning (Morris, 1989; Staubli et al. , 1989; Flood et al. , 1990; Collinridge and Bliss, 1995).It is likely that conditioned fear learning depends on CS–US pairing mediated by NMDA receptors within the BLA (Miserendino et al. , 1990; Fanselow and LeDoux, 1999). Extinction also appears to require active, NMDA-dependent learning within the amygdala. This was demonstrated by blockage of extinction by microinjections of APV into the BLA in both fear-potentiated startle (Fall s and Davis, 1992) and freezing paradigms (Lee and Kim, 1998). Furthermore, systemic administration of a different NMDA antagonist, MK801, blocks the extinction process in a range of different learning paradigms (Cox and Westbrook, 1994; Baker and Azorlosa, 1996; Kehoe et al. , 1996).Recently, DCS, a partial agonist acting at the strychnine-insensitive glycine-recognition site of the NMDA receptor complex, has repeatedly been shown to facilitate learning in various cue and context association paradigms (Monahan et al. , 1989; Flood et al. , 1992; Thompson and Disterhoft, 1997). Walker et al. (2002) reported the ? rst evidence that DCS facilitates extinction of learned fear. Since then, further studies con? rmed and elaborated this early ? nding (Ledgerwood et al. , 2003, 2004; Ressler et al. , 2004). These studies reported that DCS is more effective at facilitating extinction when given after extinction training, rather than before. They interpret these ? dings as evidence that DCS facilitates the consolidation of a new memory acquired during extinction. It is important to note that although some studies have shown DCS to be effective in improving memory impairment due to Alzheimer’s disease (Schwartz et al. , 1996; Tsai et al. , 1999) and schizophrenia (Javitt et al. , 1994; Goff et al. , 1999), other studies found little or no improvement (Tsai et al. , 1998; van Berckel et al. , 1999). This may be related to the fact that acute treatment with DCS may have a more pronounced facilitation than chronic treatment (Quartermain et al. , 1994; Ledgerwood et al. , 2003; Richardson et al. , 2004). Ledgerwood et al. (2003, 2004) reported that DCStreated animals fail to exhibit reinstatement effects.That DCS enhances extinction may be through some processes different from extinction induced by repeat representation of CS. Lin et al. (2003) investigated the similarities and differences between consolidation of conditioning and consolidation of extinction. They fo und that both processes depend on activation of NMDA receptors, PI-3K, MAPK, and require synthesis of new proteins within the amygdala. They also found that different characteristics show differential sensitivity to the transcription inhibitor actinomycin D. Our results were consistent with the model that the extinc- tion process involved active learning of new inhibitory associations.Here we showed that DCS facilitation of extinction could be blocked by actinomycin D and anisomycin. These seemingly con? icting results could be attributable to our extinction protocol. Our protocol resembled betweensession extinction, presumably corresponding to long-term extinction memory. In addition, we used DCS to facilitate the extinction process and tested the animals in a drug free condition. Acquisition or consolidation of long-term memory requires activation of protein kinase, transcription of genes, new protein synthesis, and synapse formation (Schafe and LeDoux, 2000). Similar mechanisms w ere involved in the DCS facilitation of extinction. The DCS activated NMDA receptors, resulted in Ca2 in? x into the cell, and led to the PI-3K and MAPK activation. Activated MAPK can translocate to the nucleus, subsequently activating transcription factors to promote gene transcription and new protein synthesis. Thus, combinations of drugs and extinction training may weaken or erase original memory. There is increasing evidence that learning of CS–US associations involves synaptic plasticity within the BLA, leading to differential activation of this circuit by sensory afferents (Davis, 1997; Rogan et al. , 1997; Lee and Kim, 1998; Fanselow and LeDoux, 1999). Our results suggested that the extinction of conditioned fear also involved NMDA-dependent plasticity, but speci? inhibitory circuits may be activated by extinction learning. We hypothesize that this newly activated inhibitory circuit would oppose conditioned excitatory pathways normally leading to activation of the cent ral nucleus of the amygdala, resulting in the elicitation of fear responses. CONCLUSION This may be the ? rst study to show that PI-3K and MAPKdependent signaling cascade and de novo protein synthesis within the BLA were essential to the DCS facilitation of the extinction of conditioned fear. Acknowledgments—The work was supported by grants from the National Science Council (NSC 90-2320-B-003-007, NSC 902320-B-006-038, NSC 93-2320-B-003-003).Our gratitude (also) goes to the Academic Paper Editing Clinic, NTNU. REFERENCES Baker J, Azorlosa J (1996) The NMDA antagonist MK-801 blocks the extinction of Pavlovian fear conditioning. Behav Neurosci 110:618–620. 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Free Essays on Emily Dickinson

EMILY DICKINSON Emily Dickinson lived in an era of Naturalism and Realism (1855-1910). She lived in a period of The Civil War and the Frontier. She was affected by her life and the era she lived in. She also had many deaths in her family and that’s part of the reason that she was very morbid and wrote about death. Emily Dickinson grew up in Amherst, Massachusetts in the nineteenth century. As a child she was brought up into the Puritan way of life. She was born on December 10, 1830 and died fifty-six years later. Emily lived isolated in the house she was born in; except for the short time she attended Amherst Academy and Holyoke Female Seminary. Emily Dickinson never married and lived on the reliance of her father. Dickinson was close to her sister Lavinia and her brother Austin her whole life. Most of her family were members of the church, but Emily never wished to become one. Her closest friend was her sister-in-law Susan. Susan was Emily's personal critic; as long as Emily was writing she asked Susan to look her poems over. Emily Dickinson was affected by her life for several reasons. One of the reasons was that she was never married, though she went through many serious relationships, she never settled down. Another reason that she was affected by her life was that her mother was not â€Å"emotionally accessible†. She was not close to her mother and never shared any of her feelings with her, which most daughters feel they can. This might have caused Emily to be very weird and strange. The Dickinson children were also raised in the Christian tradition, and were expected to take up their father’s religious beliefs and values without any fighting or arguing. Emily did not like than she can not chose for herself her own beliefs and religion. Emily did not enjoy the popularity and excitement of the public life, unlike her father. So she began to pull away from it. In the presence of strangers Emily could be shy, silent o... Free Essays on Emily Dickinson Free Essays on Emily Dickinson The authors of the two poems are Emily Dickinson and Walt Whitman. The name of Dickinson’s poem is â€Å"This quiet dust was gentlemen and ladies.† The name of Walt Whitman’s poem is â€Å"Song Number 6.† I believe that these two poems are different in a lot of ways, but they are alike in that they both speak of death. The poems have few similarities. Although both Dickinson and Whitman seem to be very interested in death and what happens after life. They seem to be intrigues in the uncertainties of death; for example, Whitman asks, â€Å"What do you think has become of the young and old/ men?† He wants to know exactly what happens after death. Dickinson also reminisces about how these people were once alive and she wonders what that did in life. She said, â€Å"And Lads and Girls/ Was Laughter and Ability and Sighing.† These poems are different in more ways than one. Emily Dickinson seems to wonder what these dead people were like while they were alive. She said, â€Å"This quit Dust was Gentlemen and Ladies/ And Lads and Girls.† Dickinson doesn’t seem to wonder about what happens after death as much as Whitman. They also had different writing styles. Whitman wrote in free verse, while Dickinson had a rhyme scheme. I like Emily Dickinson’s poem better because it was short and to the point. I like that Dickinson is interested in what these people were like before they passed on, because I have wondered that exact same thing more than once. I also like that Dickinson used a rhyme scheme, because that makes the poem easier to read.... Free Essays on Emily Dickinson EMILY DICKINSON Emily Dickinson lived in an era of Naturalism and Realism (1855-1910). She lived in a period of The Civil War and the Frontier. She was affected by her life and the era she lived in. She also had many deaths in her family and that’s part of the reason that she was very morbid and wrote about death. Emily Dickinson grew up in Amherst, Massachusetts in the nineteenth century. As a child she was brought up into the Puritan way of life. She was born on December 10, 1830 and died fifty-six years later. Emily lived isolated in the house she was born in; except for the short time she attended Amherst Academy and Holyoke Female Seminary. Emily Dickinson never married and lived on the reliance of her father. Dickinson was close to her sister Lavinia and her brother Austin her whole life. Most of her family were members of the church, but Emily never wished to become one. Her closest friend was her sister-in-law Susan. Susan was Emily's personal critic; as long as Emily was writing she asked Susan to look her poems over. Emily Dickinson was affected by her life for several reasons. One of the reasons was that she was never married, though she went through many serious relationships, she never settled down. Another reason that she was affected by her life was that her mother was not â€Å"emotionally accessible†. She was not close to her mother and never shared any of her feelings with her, which most daughters feel they can. This might have caused Emily to be very weird and strange. The Dickinson children were also raised in the Christian tradition, and were expected to take up their father’s religious beliefs and values without any fighting or arguing. Emily did not like than she can not chose for herself her own beliefs and religion. Emily did not enjoy the popularity and excitement of the public life, unlike her father. So she began to pull away from it. In the presence of strangers Emily could be shy, silent o... Free Essays on Emily Dickinson In 1874, Dickinson’s father died. This left her deeply distressed. Her mother suffered paralysis a year later and was invalid for the rest of her life. It was during this time that Dickinson cared for her mother and really came to love her. Dickinson’s mother died in 1882. While growing up, the Dickinson children were devoted to one another, even though the house lacked joy. The children had no relationship with their mother, and their father was stern and involved with his work (Donoghue 452). Dickinson spent the first twenty-five years of her life secluded from all but her closest friends. She had many intense intellectual friendships with several men in succession. She quaintly referred to these men as her tutors. The first of these was Benjamin F. Newton. He was a law student in her father’s office who encouraged her to read and take her talent for writing poetry seriously. Because of Newton’s early death, she looked to Reverend Charles Wadsworth for guidance. â€Å"She soon came to regard him as her dearest ‘earthly friend,’ and for purposes of poetry created in his image the ‘lover’ whom she was never to know except in imagination† (Hart 224). Wadsworth’s departure from her life is greatly associated with her increasing fascination with poetry. This prompted her correspondence with T.W. Higginson. His kind words and support helped her through lonely years. She also befriended Samuel Bowles, Dr. J.G. Holland, and H elen Hunt Jackson. These were the few individuals who Dickinson allowed to read some of her works (Hart 224). Dickinson strongly resisted the doctrine of â€Å"election.† This is the view that some were marked from birth for salvation and others were condemned to Hell. At Mount Holyoke, Dickinson was among those who had not been redeemed. She was one of three not saved. To be considered such, she was expected to declare some religious experience. She refused to do so, just to gain a social acceptance. ... Free Essays on Emily Dickinson Emily Dickinson Emily Elizabeth Dickinson was born to Edward, and Emily Norcross Dickinson on December 10th, 1830, in Amherst, Massachusetts. It was believed that during her childhood, the household was a joyless, restrictive life. Scholars believed that it was dominated by a tyrannical father, but since then, that vision has been modified. Now, it appears that the Dickinson children’s lives were very normal. They spent their days with the usual childhood activities, playing games and pranks, also splashing through mud puddles and exploring the countryside. As they grew older, they went to parties and fretted over infatuations and complained about household chores. Emily had two other siblings. Lavina, her sister was two years younger than Emily, and Austin, who was one year older, was her brother, and her best friend. At 17, Emily enrolled at Mount Holyoke Female Seminary in South Hadley, Massachusetts. She left ten months later for an unknown reason. When she quit, it marked the end of her Formal education but kept teaching herself, studying poetry, and other writings. She even knew much of the Bible by heart. She felt very strongly about how poetry made her feel. She once said to a friend, â€Å"If I read a book and it makes my whole body so cold no fire ever can warm me, I know that is poetry. If I feel physically as if the top of my head were taken off, I know that is poetry.† Emily attempted to get her works published in the early 1860’s. She sent her writings to Thomas Wentworth. She sent four of her poems to him in her very first attempt to be a publishing poet. He knew she had raw talent, an his response was significant. However, her rough rhythms and imperfect rhymes were counting big against her. He suggested she change that as well as her spelling and grammar. Emily chose not to publish anything then. The death of her father marked the beginning of Emily’s physical reclusiveness from the world. But the separat... Free Essays on Emily Dickinson Emily Dickinson was born on December 10, 1830 in Amherst Massachusetts. She had a younger sister named Lavina and an older brother named Austin. Her mother Emily Norcross Dickinson, was very dependent on her family and was seen by Emily as a poor mother. Her father was a lawyer, a Congressman, and the Treasurer for Amherst College. Emily’s grandfather was also known for building the brick mansion in Amherst. That house was later known as the Homestead. Unlike her mother, Emily loved and admired her father. Since the family was not emotional, they lived a quiet secure life. They rarely shared their problems with each other so Emily had plenty of privacy for writing during her childhood. As she matured she began to notice the gap between herself and her family’s religious belief's. She refused to accept the god of her parents and made it know that accepting things the way they are was not her style. Emily and her family attended The First Congregational Church on a regular basis. Emily did not like going to church because she didn’t think of herself as being very religious. She refused to believe that Heaven was a better place than Earth and eventually moved away from the church. Emily saw herself as a woman who had her own way of thinking. By the time she was twelve, her family moved to a house on Pleasant Street where they lived from 1840 to 1855. Emily was already writing letters, but wrote most of her poetry in this home. Emily only left home to attend Mount Holyoke Female Seminary for two semesters. During this time Emily was very energetic and had few freinds. She also was involved town social events. Even though her stay there was brief, she impressed her teachers with her courage and directness. They felt that her writing was very impressive. At the age of twenty-one, Emily and her family moved to the Dickinson Homestead on Main Street. This move proved to be very difficult for Emily. This was difficult for Emily ... Free Essays on Emily Dickinson Much Madness is Divinest Sense â€Å"Much Madness Is Divinest Sense† was published in Emily Dickinson’s first collection, which was simply called Poems. This poem concentrates on society’s judgmental views of non-conformists. In this essay, I will be explicating this poem line by line paying close attention to the unique capitalization, rhythm, rhyme, alliteration, and wordplay. Much Madness is divinest Sense- To a discerning Eye- Much Sense- the starkest Madness- ‘Tis the Majority (1-4) The â€Å"Eye† (2) is a vague image. Dickinson utilizes a synecdoche to further the image of the â€Å"Eye† to be representational of a â€Å"wise† person who has the power to label behavior â€Å"normal† or â€Å"mad†. Much Madness is divinest Sense- To a discerning Eye- Much Sense- the starkest Madness- ‘Tis the Majority (1-4) The poem opens with a statement that is a paradox. The capitalization of â€Å"Much Madness† (1) draws the readers focus to and emphasizes the juxtaposition of â€Å"Much Madness† (1) and â€Å"divinest Sense† (1). Although these words are contradictory, Dickinson finds a relationship in meaning; while society views nonconformists as mad and conformists as sane, it is actually the nonconformist who is sane and the conformists who are mad. Questions that may arise with the first two words in this line might concern what she means by â€Å"madness.† Is Dickinson referring to insanity or anger? There is a difference in the degree of madness that’s acceptable and combining â€Å"Madness† (1) with â€Å"divinest† suggests that not only madness is an important issue but also that it is connected with the divine on some level. The capitalization of the word â€Å"Eye† (2) in the second line emphasizes the pun on the pronoun â€Å"I†. When Dickinson writes, â€Å"To a discerning Eye† (2) she is specifically referring to the speaker of the poem. The speaker is the â€Å"discerning I† (2), they are the one ... Free Essays on Emily Dickinson Emily Dickinson was considered to be one of the greatest American lyric poets that ever lived. Emily was born and raised in Amherst, Massachusetts. She was raised in a traditional New England. She lived a very sheltered and exclusive life, rarely venturing out of her bedroom. Emily stayed in her room and wrote poetry, and read books all day. Emily never had any of her poems published, because she hated fame, and did not want to be acknowledged for her work. Emily Dickinson was born December tenth 1830. Her father Edward Dickinson, was a successful lawyer, a member of congress, and for many years treasurer of Amherst College. Emily’s mothers name was Emily Norcross Dickinson, she was a submissive timid woman. (Emily 352) Emily had an older brother and a younger sister. Emily’s brother William Austin was a lawyer. William and Emily were not to close relationship wise; she never really opened up to anyone. Her younger sister Lavenia was in a way like Emily, she also never left the house. Lavenia was the chief housekeeper of her household. Neither Emily nor Lavenia ever married. Emily’s brother Austin married a woman by the name of Susan Huntington, in 1856. (Skiba 216) Emily used to go to school with Susan. Over the years Emily grew very close to Susan, Emily considered her to be her best friend. Susan lived right next door to Emily; she was a very big influence in Emily’s life. Many other writers such as John Keats, Ralph Waldo Emerson, Isaac Watts and many other biblical poets also influenced Emily. (Emily 352). In Emily’s childhood she was shy and different from the others. Emily did attend school, before she became completely unsocial. She went to Amherst Academy for a few years, before attending Mt. Holyoak College. (Skiba 216) Emily loved to read especially if it had anything to do with Shakespeare or Religion. While at college she majored in Chemistry and Astronomy. (Dickinson, New Book 153) Almost ... Free Essays on Emily Dickinson Emily Dickinson, recognized as one of the greatest American poets of the nineteenth century, was born December 10, 1830 in Amherst, Massachusetts (Benfey, 1). Dickinson’s greatness and accomplishments were not always recognized. In her time, women were not recognized as serious writers and her talents were often ignored. Only seven of her 1800 poems were ever published. Dickinson’s life was relatively simple, but behind the scenes she worked as a creative and talented poet. Her work was influenced by poets of the seventeenth century in England, and by her puritan upbringing. Dickinson was an obsessively private writer. Dickinson withdrew herself from the social contract around the age of thirty and devoted herself, in secret, to writing. She never married, finding in her poetry, reading, gardening, and close friendships, a rich and fulfilling life. Emily grew up with a privileged childhood. She was the eldest daughter of Edward Dickinson, a successful lawyer, member of congress, and for many years treasurer of Amherst College. Her father gave here the time, and literary education, as well as confidence to try her hand at free verse. Emily’s mother, Emily Norcross Dickinson, was a submissive, timid housewife dedicated to her husband, children, and household chores. The Dickinson’s only son, William Austin, also a lawyer, succeeded his father as treasurer of the college. Their youngest child, Lavina, was the chief housekeeper and, like her sister, Emily, remained a home, unmarried, all her life. A sixth member who was added to the family in 1856 was Susan Gilbert, a schoolmate of Emily’s, who married Austin and moved into the house next door the Dickinson home which they called Homestead. Emily and Susan were very close friends and confidantes, until Susan and Austin’s marriage. It was at this time tha t Susan stopped respo! nding to the notes and poems that were often exchanged between the two ( ). Emily’s letters to Su...