Learning and Memory

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Biology 202
1998 First Web Reports
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Learning and Memory

Ruchi Rohatgi

Learning and memory are not unitary processes. Learning is the process by which new information is acquired; memory is the process by which that knowledge is retained. Learning can be divided into two types: 1)Explicit memory is the conscious acquisition of knowledge about people, places and things. It occurs in the highly developed vertebrate brain ,mainly in the diencephalic structure (1). 2) Implicit memory is the non conscious learning of motor skills and other tasks. It does not depend on the temporal lobe, but involves the sensory, motor associated pathways in the expression of learning process. This type of memory can be studied in higher invertebrates whereas explicit learning is only studied in mammals (2).

After reviewing the enormous amount of information pertaining to memory and learning, I decided to focus on two areas of interest: the actual mechanism of learning and the process of consolidation which relates to how something that is learned is then stored as memory. The first area of interest involving learning has been elucidated by the concept of long term potentiation (LTP) in mammals and vertebrates and the second related area of consolidation has been elucidated by an invertebrate model of Aplysia.

Long term potentiation can be defined as a long lasting increase in synaptic effectiveness which follows from high frequency of stimulation of afferent fibers. Although LTP occurs throughout the nervous system, it's focus has mainly been in the hippocampus which is involved in the formation of certain memories (1). Furthermore, LTP has been found to occur in not only the mammalian brain but also in other vertebrates such as the goldfish, bullfrog, bird and lizard. Characteristics of LTP commonly associates it with memory storage, especially in the Hebbian descriptions of memory formation. The idea behind this is consistent with what a memory mechanism should and can possess. Donald Hebb wrote, "When an axon of cell A...excites cell B and repeatedly takes part in firing it, some growth process or metabolic change takes place in one or more cells so that A 's efficiency as one of the cells firing B is increased (4)" Thus, memory is likely to involve a strengthening of synaptic activity. This "Hebb's rule closely resembles the definition of LTP in that learning is accompanied by an increase in the efficiency of communication between neurons.

After reviewing information, it seems that LTP implication in learning has been accepted as a model because it makes sense and nothing better has been proposed. It is a long standing theory that has come under various controversy. However, conflicting experimental results have lead some to believe that LTP is involved in only some learning. Furthermore, many scientists argue that statements such as "learning underlies learning and memory" should be replaced by "enhanced synaptic efficacy underlies memory storage (3)" Shors and Matzel believe that LTP mainly acts by "altering the organisms responsiveness, or perception of environmental stimuli." They proposed the argument that certain environmental cues are represented in the brain as a pattern of synaptic responses and LTP acts to magnify these responses in order to allow a more rapid detection of stimuli (3).

Many studies have been done with LTP in learning. Certain drugs or other genetic manipulations that block hippocampal LTP facilitate performance in some tasks but impair performance in other tasks. However, a number of studies have found evidence that LTP -like increases in synaptic potency occur in the hippocampus during learning of tasks. Some tasks include spatial learning, associative eye blink conditioning (as shown in rabbits) and olfactory discriminations. Nevertheless, it has been shown that artificial induction of LTP has no clear effect on learning new tasks. Thus, maybe the induction of LTP is not a sufficient enough condition for the storage of new memories and other mechanisms besides LTP are involved in this storage (4).

Models of the invertebrate Aplysia have demonstrated that memory storage are represented at the level of individual neurons by changes in the strength and structure of synaptic connections. Long term memory, lasts for days, weeks and is associated with the growth of new synaptic connections activated by altered gene expression and new protein synthesis (5).

Sensitization is nonassociative learning where the animal learns about the properties of a single harmful stimulus. In Aplysia, sensitization of the gill and siphon withdrawal reflex can be induced by a strong stimulus applied to another site, such as the tail or neck. Facillatory interneurons are then activated which synapse on sensory neurons and strengthen synaptic connection between the sensory neurons and target cells. Behavioral memory for sensitization of the gill and siphon withdrawal reflex is graded. A single stimulus to the tail gives rise to short term sensitization whereas repeated stimulation produces long term behavioral sensitization (5,6).

Short and long term memory sensitization is represented by monosynaptic connections between sensory neurons. Serotonin (5 HT), a modulatory neurotransmitter normally released by sensitizing stimuli, can substitute for the shock to the neck or tail. For example, a single application of 5 HT produces short term changes in areas for synaptic effectiveness whereas more applications of 5-HT produce long term changes (7).

Short term cellular changes differ from long term cellular changes in that 1) short term changes involves only modification of pre existing proteins and alterations of pre existing connections. The short term process does not involve ongoing macromolecule synthesis. This is known since short term change is not blocked by transcription/ translation inhibitors. However these inhibitions do block induction of long term changes. Thus there must be a critical time in learning where proteins and RNA are required to change short term changes into long term changes. 2)Long term process involves a structural change which is not seen in the short term. In long term processes, there is a growth in new synaptic connections by sensory neurons onto follower cells (8).

The long term facilitation in Aplysia is similar to the long term potentiation (LTP) in mammalian hippocampus. Studies have found that the start of LTP is associated with increased mRNA expression encoding transcription factors and other proteins needed for growth. This shows that long term changes in both mammals and Aplysia are linked to gene induction which leads to synaptic growth (3,4).

In conclusion, the structural changes implicated in long term memory are due to new protein and mRNA synthesis. These changes in transcription and translation can be initiated by repeated exposure to modulatory transmitters (5 HT) which mimic the effects of hormones and growth factors. Furthermore, through second messenger systems that regulate gene expression, modulatory transmitters utilized for learning can initiate synaptic growth.

WWW Sources

1) dead link



4) Long-Term Potentiation: What's Learning Got To Do With It?

5) Structure of the Network Mediating Siphon-Elicited Siphon Withdrawal in Aplysia.



8) Long-Term Effects of Axotomy on Excitability and Growth of Isolated Aplysia Sensory Neurons in Cell Culture: Role of cAMP.



Comments made prior to 2007

I have a new book and Web site on what science reveals about improving memory. The book is entitled "Thank You Brain For What You Remember. What You Forgot Was My Fault." Although the book is lay-audience oriented, I do discuss relevant experiments and their applications to everyday memory. In general, there are some 150 specific ideas for improving one's memory. The book's Web site is at http://thankyoubrain.com

The Web site features an advice column and I am starting a blog on summarizing memory research. There is also information about memory workshops that I give ... Bill Klemm, 27 July 2005


the j..w clan's picture

should i continue seeing my phsyc

i left my treatment after many years with the mental health team because i felt that the treatment was inafective. i was formely diagnosed with D.i.d by a phycoligist who had even at the time when peopl were a lot more sceptical. i had been in the mental health system a long time and when i was seeing that first phyc who dianosed me at first things exculated and just when she got the team , inner family finally working at the thought of co-operation , eknowledging other members and was talking to us about possible intergration i and them were getting well enough to even reduse the amount of anti-sycotic modo s that mental health team and the pyhc hospital had me on ,this wonderfull talented , remarcable pysc called ros gribble died and she was ( and i mean practucally)on her death bed and wanted to make sure she left me in the care of a colleage whom she trusted to continue on from mental health.,
, whom even took me to her funeral decided only after a couple of sessions that he would re - diagnose the miss diagnoses i suffered under for so many lost years, cutting , suicide attempts and even an attempted murder charge,the police shot me twice to prevent it.I started to see a good christian physc who sussed srtaight away something else was up sent me for further help to the pysc i see now . its like everyone is to scared to use the word D.D.D they would feel much more comfortable to call it even schitzaprheniabut i think this pysc may have sussed us out of hiding some of us hope cause we remember ross gribble but what if he hasnt. my patner just left me a few dys ago due to the difficulties . so this pysc saw me friday due to my acute messy uncoperative head and because im thinking were sussed out i stopped the session mid way, i knew with in an instance what has been goig on for me . so many people trying to get rid of inner voices that have been busting to be pushed back in , even called by me what their not .my life itself is in great risk if i dont very soon get the pysc not only to recognise but to have enough competence and skill to save this very life. i feel if dont get the right help or if this pysc hasnt busted me ,her him them us then she the one of anger and agression will kill us . i was sxually assulted 3 years ago and even with the help of vocsl i am being victimised all over again due to inafficint police work as well as the perpetraitor s continuak harrasment 3 years on . do you blame my partner for leaving i dont some do within and the j..w clsn im allowing to run a muck easy to let them withouy a partner thinkinging that im just mental every moments a pump with us.so at the moment its like continual pop ups , in and out . one moment this strong feeling next that , one moment in lafter as a immature child but we are being threatened by death again, she says its her choice we say its ours then she breaks into the death rage crying not tears just raw hate and anger . shes been dunped but she dumped us . wre spose to be a team that dosnt hate one or the other . sorry i fell into ranting but im desprate . what happens when i see my psyc again this week ? what happens if he hasnt cottened on were scared of her she getting harder to stop and now the , her not hers but the other her the soft one , the cruel angry one will maybe now get her onside that the partners gone.should we risk goig back to the pysc and he dosnt have our system busted cause in the session we dont know who will go.had to tell you everything incase the team dosent even make it . had to tell something rather then someone . sorry for your ear . just sop sorry . i dont even know i should be talking with such oppeness i dont want to cause trouble ,be in trouble , not believed or ridicled surly we couldnt take being shoveed back to a pretend pressurised port hole . sooy if wev e freaked you. me them us jen the j..w clan sorry to you

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