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6.4: Some Neurobiological Facts about Memory

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    In this section, we will first consider how information is stored in synapses and then talk about two regions of the brain that are mainly involved in forming new memories, namely the amygdala and the hippocampus. To show what effects memory diseases can have and how they are classified, we will discuss a case study of amnesia and two other common examples for amnesic diseases: Karsakoff’s amnesia and Alzheimer’s disease.

    Information storage

    The idea that physiological changes at synapses happen during learning and memory was first introduced by Donald Hebb.[18] It was in fact shown that activity at a synapse leads to structural changes at the synapse and to enhanced firing in the postsynaptic neuron. Since this process of enhanced firing lasts for several days or weeks, we talk about Long Term Potentiation (LTP). During this process, existing synaptic proteins are altered and new proteins are synthesized at the modified synapse. What does all this have to do with memory? It has been discovered that LTP is most easily generated in regions of the brain which are involved in learning and memory - especially the hippocampus, about which we will talk in more detail later. Donald Hebb found out that not only a synapse of two neurons is involved in LTP but that a particular group of neurons is more likely to fire together. According to this, an experience is represented by the firing of this group of neurons. So it works according to the principle: “what wires together fires together”.


    The amygdala is involved in the modulation of memory consolidation.


    Following any learning event, the Long Term Memory for the event is not instantaneously formed. Rather, information regarding the event is slowly assimilated into long term storage over time, a process referred to as memory consolidation, until it reaches a relatively permanent state. During the consolidation period, memory can be modulated. In particular, it appears that emotional arousal following a learning event influences the strength of the subsequent memory for that event. Greater emotional arousal following a learning event enhances a person's retention of that event. Experiments have shown that administration of stress hormones to individuals, immediately after they learn something, enhances their retention when they are tested two weeks later. The amygdala, especially the basolateral nuclei, is involved in mediating the effects of emotional arousal on the strength of the memory for the event. There were experiments conducted by James McGaugh on animals in special laboratories. These laboratories have trained animals on a variety of learning tasks and found that drugs injected into the amygdala after training affect the animal’s subsequent retention of the task. These tasks include basic Pavlovian Tasks such as Inhibitory Avoidance, where a rat learns to associate a mild footshock with a particular compartment of an apparatus, and more complex tasks such as spatial or cued water maze, where a rat learns to swim to a platform to escape the water. If a drug that activates the amygdala is injected into the amygdala, the animals had better memory for the training in the task. When a drug that inactivated the amygdala was injected, the animals had impaired memory for the task. Despite the importance of the amygdala in modulating memory consolidation, however, learning can occur without it, although such learning appears to be impaired, as in fear conditioning impairments following amygdala damage. Evidence from work with humans indicates a similar role of the amygdala in humans. Amygdala activity at the time of encoding information correlates with retention for that information. However, this correlation depends on the relative "emotionality" of the information. More emotionally-arousing information increases amygdalar activity, and that activity correlates with retention.


    Psychologists and neuroscientists dispute over the precise role of the hippocampus, but, generally, agree that it plays an essential role in the formation of new memories about experienced events (Episodic or Autobiographical Memory).


    Some researchers prefer to consider the hippocampus as part of a larger medial temporal lobe memory system responsible for general declarative memory (memories that can be explicitly verbalized — these would include, for example, memory for facts in addition to episodic memory). Some evidence supports the idea that, although these forms of memory often last a lifetime, the hippocampus ceases to play a crucial role in the retention of the memory after a period of consolidation. Damage to the hippocampus usually results in profound difficulties in forming new memories (anterograde amnesia), and normally also affects access to memories prior to the damage (retrograde amnesia). Although the retrograde effect normally extends some years prior to the brain damage, in some cases older memories remain intact - this sparing of older memories leads to the idea that consolidation over time involves the transfer of memories out of the hippocampus to other parts of the brain. However, researchers have difficulties in testing the sparing of older memories and, in some cases of retrograde amnesia, the sparing appears to affect memories formed decades before the damage to the hippocampus occurred, so its role in maintaining these older memories remains controversial.


    As already mentioned in the preceding section about the hippocampus, there are two types of amnesia - retrograde and antrograde amnesia.


    Different types of Amnesia

    Amnesia can occur when there is damage to a number of regions in the medial temporal lobe and their surrounding structures. The patient H.M. is probably one of the best known patients who suffered from amnesia. Removing his medial temporal lobes, including the hippocampus, seemed to be a good way to treat the epilepsy. What could be observed after this surgery was that H.M. was no longer able to remember things which happened after his 16th birthday, which was 11 years before the surgery. So given the definitions above one can say that he suffered retrograde amnesia. Unfortunately, he was not able to learn new information due to the fact that his hippocampus was also removed. H.M. therefore suffered not only from retrograde amnesia, but also from anterograde amnesia. His Implicit Memory, however, was still working. In procedural memory tests, for example, he still performed well. When he was asked to draw a star on a piece of paper which was shown to him in a mirror, he performed as bad as every other participant in the beginning. But after some weeks his performance improved even though he could not remember having done the task many times before. Thus, H.M.’s Declarative Memory showed severe deficits but his Implicit Memory was still fine. Another quite common cause of amnesia is the Korsakoff’s syndrome or also called Korsakoff’s amnesia. Long term alcoholism usually elicits this Korsakoff’s amnesia due to a prolonged deficiency of vitamin B1. This syndrome is associated with the pathology of the midline diencephalon including the dorsomedial thalamus. Alzheimer’s disease is probably the best known type of amnesia because it is the most common type in our society. Over 40 percent of the people who are older than 80 are affected by Alzheimer’s disease. It is a neurodegenerative disease and the region in the brain which is most affected is the entorhinal cortex. This cortex forms the main input and output of the hippocampus and so damages here are mostly severe. Knowing that the hippocampus is especially involved in forming new memories one can already guess the patients have difficulties in learning new information. But in late stages of Alzheimer’s disease also retrograde amnesia and even other cognitive abilities, which we are not going to discuss here, might occur.


    This figure shows the brain structures which are involved in forming new memories

    Final checklist of what you should keep in mind
    1. Why does memory exist?
    2. What is sensory memory?
    3. What is the distinction between Short Term memory and Working Memory?
    4. What is Long Term Memory and which brain area(s) are involved in forming new memories?
    5. Remember the main results of the theory (For example: What does the Filter Theory show?)
    6. Don’t forget why we forget!

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