The Neural Basis of Learning and Memory

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Not all types of memory have the same neural mechanisms or, as we have seen, involve the same parts of the brain. The prefrontal cortex of the frontal lobes (see Figure 13-9), is active in both components—the storage and executive processes—of working memory, but discrete regions of prefrontal cortex deal with specific kinds of information. Thus, one area of the prefrontal cortex encodes information about verbal material such as attaching names to objects or events, a different area deals with spatial memories such as how to get from one place to another, and yet another area deals with memories of events. Still other areas deal with the executive processes. Cortical areas other than the prefrontal cortex are involved in working memory as well.

Recall that the prefrontal cortex is also the destination of a major branch of the mesolimbic dopamine pathway, a pathway mentioned earlier in the context of directed attention. Directed attention is a critical component of working memory—we do not remember what we have not paid attention to—and these two mechanisms interact in prefrontal cortex. Recall, too, that dopamine is a major neurotransmitter implicated in directed attention; thus, drugs that are dopamine antagonists—drugs such as those used for schizophrenia, for example—interfere with working memory. Prefrontal cortex is also the target of a cholinergic

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Consciousness and Behavior CHAPTER THIRTEEN

Consciousness and Behavior CHAPTER THIRTEEN

neural system that originates in the brainstem as a component of the reticular activating system.

But what is happening during the memory formation on a cellular level? Conditions such as coma, deep anesthesia, electroconvulsive shock, and insufficient blood supply to the brain, all of which interfere with the electrical activity of the brain, interfere with working memory. Thus, it is assumed that working memory requires ongoing graded or action potentials. Working memory is interrupted when a person becomes unconscious from a blow on the head, and memories are abolished for all that happened for a variable period of time before the blow, so-called retrograde amnesia. (Amnesia is defined as the loss of memory.) Working memory is also susceptible to external interference, such as an attempt to learn conflicting information. On the other hand, long-term memory can survive deep anesthesia, trauma, or elec-troconvulsive shock, all of which disrupt the normal patterns of neural conduction in the brain. Thus, working memory requires electrical activity in the neurons, but the question remains: What happens next?

The problem of how exactly memories are stored in the brain is still unsolved, but some of the pieces of the puzzle are falling into place. One model for memory is long-term potentiation (LTP), in which certain synapses undergo a long-lasting increase in their effectiveness when they are heavily used. Long-term po-tentiation results from increased activation of glutamate receptors on the postsynaptic cell, which opens Ca2+ channels in the receptor, causing an increase of cytosolic calcium. The calcium enhances the enzymatic formation in the postsynaptic cell of nitric oxide, which diffuses back across the synapse to enhance the effectiveness of the synapse. An analogous process, long-term depression (LTD), decreases the effectiveness of synaptic contacts between neurons.

Other models for memory encoding involve feedback loops of second-messenger molecules in postsyn-aptic cells, which can sustain activity in these cells long after the membrane-receptor activity ceases. Moreover, it is generally accepted that memory encoding involves processes that alter gene expression and result in the synthesis of new proteins. This is achieved by a cascade of second messengers that activate genes in the cell's DNA. Yet another class of memory models is based on the idea that memory is encoded by structural changes in the synapses (for example, by an increase in the number of receptors on the postsynaptic membrane). This ability of neural tissue to change because of its activation is known as plasticity.

Additional Facts Concerning Learning and Memory

Certain types of learning depend not only on factors such as attention, motivation, and various neurotrans-

TABLE 13-5 General Principles about Learning and Memory

1. There are multiple memory systems in the brain.

2. Working memory requires changes in existing neural circuits, whereas long-term memory requires new protein synthesis and growth.

3. These changes may involve multiple cellular mechanisms within single neurons.

4. Second-messenger systems appear to play a role in mediating cellular changes.

5. Changes in the properties of membrane channels are often correlated with learning and memory.

Adapted from John M. Beggs et al. "Learning and Memory: Basic Mechanisms," in Michael J. Zigmond, Floyd E. Bloom, Story C. Landis, James L. Roberts, and Larry R. Squire, eds., Fundamental Neuroscience, Academic Press, San Diego, CA, 1999.

mitters but also on certain hormones. For example, the hormones epinephrine, ACTH, and vasopressin affect the retention of learned experiences. These hormones are normally released in stressful or even mildly stimulating experiences, suggesting that the hormonal consequences of our experiences affect our memories of them.

Two of the opioid peptides, enkephalin and en-dorphin, interfere with learning and memory, particularly when the lesson involves a painful stimulus. They may inhibit learning simply because they decrease the emotional (fear, anxiety) component of the painful experience associated with the learning situation, thereby decreasing the motivation necessary for learning to occur.

Memories can be encoded very rapidly, sometimes after just one trial, and they can be retained over extended periods. Information can be retrieved from memory stores after long periods of disuse, and the common notion that memory, like muscle, atrophies with lack of use is not always true. Also, unlike working memory, memory storage apparently has an unlimited capacity because people's memories never seem to be so full that they cannot learn something new. Although we have mentioned specific areas of the brain that are active in learning, we want to stress at this time the following point: Memory traces are laid down in specific neural systems throughout the brain, and different types of memory tasks utilize different systems. For in even a simple memory task, such as trying to recall a certain word from a previously seen word list, different specific parts of the brain are activated in sequence. It is as though several small "processors" are linked together in a memory system for specific memory tasks.

Some general principles about learning and memory are summarized in Table 13-5.

PART TWO Biological Control Systems

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART TWO Biological Control Systems

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  • Declan
    What is the neural basis for learning and memory called?
    8 years ago

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