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Memory and Learning

Tracie Timme

 

MEMORY AND LEARNING

An academic paper by

Tracie L. Timme – Online Counselor and Therapist

 

This paper is about memory and learning, and how it is connected.  This paper will describe the role that memory plays in classical conditioning, instrumental conditioning, and the role it plays in the social learning theory.  We all have memories.  To learn something may be considered a memory for what was learned.  We can learn by being conditioned to respond in a certain way.  We can be taught that if we pass our tests in school, we will be rewarded with ice cream, or if we do badly on our tests we will have something taken away, classical conditioning.  We can learn from how a situation turns out according to our actions.  We can learn that if put things where they belong, we can find more easily, or we can learn that if we leave things just laying around we will have more difficulty finding them again, instrumental conditioning.  We can pick things up by just being with other people.  If we visit friends or family in the south, we can come home with somewhat of a southern accent, or we might catch ourselves saying things that we would not normally say, social learning theory.

Once you learn something, it is in your memory somewhere.  Learning is when you gain knowledge of something (Terry, 2009).  Memory is that knowledge that you have acquired that is recalled.  Short-term memory is brief and generally forgotten within 15 – 30 seconds if it is not rehearsed.  Long-term memory lasts longer and is stored more permanently (Terry, 2009).  When you learn something, you just know it, like how to read a map.  When you memorize something, you remember it for a specific reason, like a grocery list.  Once you use that list, some components from the list disappear and are forgotten.

Hoarders Just throw it all away!Learning and memory happen every day whether we realize it or not.  We learn and memorize things through classical conditioning, instrumental conditioning, and most definitely through social learning theory.  Classical conditioning is when at least two events, possibly more are connected in a relationship.  Classical conditioning happens when there is a difference in the response to one of the events, thus showing something was learned (Terry, 2009).  In classical conditioning, there are four components and they are acquisition, extinction, generalization, and discrimination.  Acquisition occurs when there is a conditioned response to the conditioning event.  Memory’s key role in this is that the response is remembered to recall and use again. Extinction occurs when there is no longer a conditioned response to the conditioning event.  The role of memory in this component is to remember a different response so the old response disappears.  Generalization occurs when there is a generalization of conditioning events to get the same conditioned response.  A response is remembered and carried over to other events that are similar.  Discrimination occurs when the conditioning events are seen differently and are able to have the conditioned response to the specific conditioning event instead of similar events.  Specific events are remembered to elicit that response.

We also learn things through instrumental conditioning.  Instrumental conditioning happens when the consequence and action are linked.  When there is an action performed, there is always an outcome, so positive and some negative.  Both positive and negative outcomes are remembered.  We remember the positive outcomes because we like they way we feel, or we like what happens as a result from our actions.  We remember the negative outcomes as well because they are negative.  We do not like to feel bad, so we remember negative outcomes in order to avoid the actions that create them.  People become addicted to substances because they like the way those substances make them feel.  Children will do whatever they can; to avoid getting caught in an act that they know will cause them to be punished.  Either the child will learn and remember that not performing that action at all, or they will learn a better way to accomplish what they want.

We all learn through social learning whether we want to admit it or not.  Some of this social learning is great, and some of the social learning we pick up is not.  Memory plays a part in social learning in that, we see our peers do something and they get rewarded for doing it.  Others we see do something, we also see get punished for doing so.  We remember how our peers were rewarded or punished.  We remember these things in order to act in the manner that our peers did, or not to behave like them.  In an office setting, we see our coworkers use the company computers for personal things.  We see them get away with it by changing the screen when a boss walks by.  Therefore, we think we can do the same.  But what we may not see, behind the scenes, is that the company is taking measures to keep track of the computer use, to be able to follow websites that are visited and from which computers they originate from.  Out of site from others, they may very well be reprimanded.  A good social learning is learning from what we see our associates do when confronted with a group of higher administrative personnel.  We can learn how their words, facial expressions, and body language affect the outcome of the meeting.  We can then recall them so we can do the same when in a similar situation.  We can also learn proper etiquette and good manners when in public places by watching how others behave.

Learning and memories happen continuously.  We are often conditioned and condition others without realizing it.  When we pick a crying child or and over excited puppy, we are conditioning them to continue that behavior.  Instrumentally we condition ourselves to eat healthier because we want to look and feel better.  Socially we learn so much we do not even know where some things came from.  Maybe a friend noticed a different walk you have all of a sudden.  We learn all the time.  Just think what we could learn if we really paid attention to the things we do, people we see, and the places we go.              

References

Terry, W.S. (2009). Learning & memory: Basic principles, processes, and procedures. (4th ed.) Boston: Pearson.

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Improving memory by suppressing a molecule that links aging to Alzheimer’s disease

In a new study conducted by the Sagol Department of Neurobiology at the University of Haifa and published recently in the Journal of Neuroscience, researchers report that they’ve found a way to improve memory by manipulating a specific molecule that is known to function poorly in old age and is closely linked to Alzheimer’s disease.

Getting bigger and biggerThe researchers even succeeded, for the first time, in manipulating the molecule’s operations without creating any cognitive impairment.

“We know that in Alzheimer’s, this protein, known as PERK, doesn’t function properly. Our success in manipulating its expression without causing any harm to the proper functioning of the brain paves the way for improving memory and perhaps even slowing the pathological development of diseases like Alzheimer’s,” said Prof. Kobi Rosenblum, who heads the lab in which the research was done.

Previous studies at the University of Haifa and other labs throughout the world had shown that the brain’s process of formulating memory is linked to the synthesis of proteins; high rates of protein production will lead to a strong memory that is retained over the long term, while a slow rate of protein production leads to weak memories that are less likely to be impressed on a person’s long-term memory and thus forgotten.

In the current study, the researchers, Dr. Hadile Ounallah-Saad and Dr. Vijendra Sharma, both of whom work in Prof. Rosenblum’s lab at the Sagol Department of Neurobiology, sought to examine the activity of a protein called elF2 alpha, a protein that’s known as the “spigot” or regulator that determines the pace of protein synthesis in the brain during memory formation.

From earlier studies the researchers knew that there are three main molecules that act on the protein and either make it work, or stop it from working. During the first stage they sought to determine the relative importance and the task of each one of the molecules that control the activity of efF2 alpha and as a result, the ability to create memories. After doing tests at the tissue and cell levels, the researchers discovered that the main molecule controlling the efF2 alpha’s activity was the PERK molecule.

“The fact that we identified the PERK as the primary controller had particular significance,” said Dr. Ounallah-Saad. “Firstly, of course, we had identified the dominant component. Secondly, from previous studies we already knew that in generative diseases like Alzheimer’s, PERK performs deficiently. Third, PERK acts on various cells, including neurons, as a monitor and controller of metabolic stress. In other words, we found a molecule that has a major impact on the process of creating and formulating memory, and which we know performs deficiently in people with Alzheimer’s disease.”

During the second stage of the study, the researchers sought to examine whether they could manipulate this molecule in rats in a way that would improve memory. To do this they used two accepted methods, one using a drug called a small-molecule inhibitor and the other making a genetic change to the brain cells using a type of virus also used in gene therapy.
After paralyzing PERK’s activity or reducing its expression through gene therapy (which was done with the help of Dr. Efrat Edry, of the University’s Center for Gene Manipulation in the Brain), the researchers measured a 30% increase in the memory of either positive or negative experiences. The rats also demonstrated improved long-term memory and enhanced behavioral plasticity, becoming better able to “forget” a bad experience. In other words, on a behavioral level it was clear that manipulating PERK by either of two methods improved memory and cognitive abilities.

When the researchers examined the tissues on a cell and molecular level, the discovered that the steps they’d taken had indeed stopped the expression of PERK, which allowed the “spigot” — the elF2 alpha protein — to perform better and increase the pace of protein synthesis. Even more, there was a clear correlation between memory function and the degree to which PERK was suppressed; the more efficiently PERK was suppressed, the better the memory function.

But the researchers faced another problem. Previous studies that had manipulated PERK in general in genetically engineered animals led to fixated behavior. “The brain operates in a most sophisticated fashion, with each action closely linked to many other actions,” said Dr. Ounallah-Saad. “In our study we succeeded in maintaining such control of the PERK that it didn’t influence the retrieval of existing memories, or do anything other cognitive damage.”

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