http://michaeldmann.net/mann18.

html

Chapter 18

LEARNING AND MEMORY

L et me begin by telling a little story. When I was a graduate student we had to take an
exam that Cornell does in an interesting way. They put you in a swivel-chair surrounded by
your committee composed of 4-5 faculty members. You are spun around, and a question
comes from the direction you face when you stop. One of the questions I was asked was,
“What will be the most important accomplishment in the field of neuroscience in the next
10 years?” Knowing that knowledge usually advances in small steps, I said that we would
gradually know more about most aspects of the field, but I didn’t expect any major
breakthroughs. To a man, the committee agreed that in 10 years we would have
a complete solution to the problem of learning and memory. The word complete was their
term, presumably meaning that we would know everything there was to know about
learning and memory. Well, at the 10-year mark, I sent them all a letter saying, “I told you
so!” Their predicted event didn’t happen. However, we have made some progress; that
progress is what this chapter is about.

Definitions
What is learning? According to Eric Kandel (2000) “Learning is the process by which we
acquire knowledge about the world.” While this definition is erudite, it doesn’t help us much
in knowing what to study. Another definition (Kimble, 1961), "Learning refers to a more or
less permanent change in behavior which occurs as a result of practice," is a little better. It
tells us that learning is more or less permanent; it won’t always be there, but often will. It
also tells us that this is something that happens because we practice–repeat something over
and over. A further definition says, “[Learning is] either a case of differential strengthening
of one from a number of responses evoked by a situation of need, or the formation of
receptor-effector connections de novo; the first occurs typically in simple selective learning
and the second in conditioned reflex learning" (Hull, 1943). It is the strengthening of existing
responses and the formation of new responses to existing stimuli that make this definition
unique. So what is learning? It isn’t clear that we have an inclusive definition. It appears that
learning is the strengthening of existing responses or formation of new responses to existing
stimuli that occurs because of practice or repetition. How much practice? Sometimes a
single practice session is sufficient as in avoidance of painful or noxious stimuli. Sometimes
a lot of practice is necessary as in learning to drive a car.

What then is memory? Again according to Kandel (2000), ". . . memory is the process by
which that knowledge of the world is encoded, stored, and later retrieved." By this
definition, memory is not a thing; it’s a process. Interesting! In another definition, "Memory
is a phase of learning . . . learning has three stages: 1. acquiring, wherein one masters a new
http://michaeldmann.net/mann18.html

activity . . . or memorizes verbal material . . . 2. retaining the new acquisition for a period of
time; and 3. remembering, which enables one to reproduce the learned act or memorized
material. In a narrower sense learning merely means acquiring skill . . ." (Sargent & Stafford,
1965). From these definitions, we see that memory has to do with keeping “knowledge”
someplace and then retrieving it when it is needed. What we don’t see here is that the
“knowledge” doesn’t have to come into consciousness. I have two cars–one with an
automatic transmission, one with a stick shift. I don’t have to bring into consciousness the
process for shifting gears when I get into the car that requires me to do that–I just do it!

Types of Memory
There are actually two basic kinds of learning and memory. One is declarative or explicit; the
other is non-declarative or implicit. Knowledge of facts–what we know about places, things
and people–and the meaning of these facts is explicit memory. These things must be
recalled into consciousness to be used. Patients who have bilateral medial temporal lobe
lesions have an inability to learn and remember items of factual knowledge. They can’t
remember people that they met the day before. They can’t remember what they did the
day before. Some people will further parcel explicit memories as episodic (we remember
events) or semantic (we remember facts). As Kandel (2000) points out, in either case the
content of all explicit memories can be expressed by declarative statements such as “I was
here yesterday” (episodic) and “The hippocampus has something to do with memory”
(semantic).

Implicit memory involves information about how to perform something; it’s recalled
unconsciously. We use implicit memory in trained, reflexive motor or perceptual skills. I
know how to drive my car; I know how to get to work. The same people with bilateral medial
temporal lobe lesions can learn simple reflexive skills–they habituate and are sensitized,
they can be classically and operantly conditioned (see later). They can learn certain
perceptual tasks. For example, they can recall a word learned previously when given only
the first few letters of the word. At the same time, they deny ever having learned the word
previously. Implicit memory is often further parceled as associative and non-associative.
There are two well-known types of non-associative learning: habituation and sensitization.
Habituation is a decrease in response to a benign stimulus when the stimulus is presented
repeatedly. A dog will be aroused when a strange tone is played. If the tone is played over
and over, the dog will eventually no longer be aroused by the tone. We say that it has
habituated. This kind of learning makes sense; it is not efficient for an organism to go on
responding to a stimulus that has no meaning. The other form of non-associative learning,
sensitization, is an enhanced response to many different stimuli after experiencing an
intense or noxious one. For example, an animal responds more vigorously to a tone of lesser
intensity once a painfully loud tone has been played. Here we say that the animal is
sensitized.
http://michaeldmann.net/mann18.html

These two forms of learning also interact. Once a response has been habituated, it can be
restored by sensitization. In this case, we say that the animal is dishabituated. As an
example: a habituated startle response to a noise can be restored by strongly pinching the
skin.

In non-associative learning, it is not necessary that the animal learns to associate the stimuli
involved (thus the name). For example, the dishabituated animal does not learn to associate
the noise with the pinch. As we shall see shortly, this is the hallmark of associative learning.
Not all forms of non-associative learning are as simple as habituation and sensitization. For
example, we learn language by imitation of people who already speak. This involves no
association of stimuli and is clearly more complicated than habituation.

In associative learning, we “learn” that two stimuli are associated with each other or that a
response is associated with a given event or has a given consequence. Perhaps important in
clinical considerations, a person can also learn that an outcome is not associated with a
response. So a person may learn that what happens to him is not related to what he does.
Two sorts of associative learning have been well studied: classical conditioning and operant
conditioning. Classical conditioning is well demonstrated by Pavlov’s famous experiment in
which he presented meat powder to a dog, causing it to salivate. He repeated the
presentation, and each time the dog salivated. If he repeatedly rang a bell just before
presenting the meat powder (they were paired), the animal came to associate the bell with
the presentation of the meat powder, and it would begin to salivate when the bell was rung.
In fact, for a while it would salivate if the bell was rung but no meat powder was presented
(they were unpaired). After a while, the bell stopped predicting the presentation of meat
powder for the dog, and it ceased salivating when it was rung. (This process is called
extinction.) It should be noted that for classical conditioning to occur the ringing of the bell
must precede the presentation of the meat powder, often by a certain critical interval of
time (of the order of 0.5 sec). One way to look at classical conditioning is to think of the bell
as becoming a signal that the meat powder is about to be presented.

In Pavlov’s paradigm, the meat powder normally elicits salivation without experimenter
intervention (it is innate or perhaps previously strongly learned), and it is called
the unconditioned stimulus (US). The response is called the unconditioned response (UR).
The bell comes to elicit salivation only after it is repeatedly paired with meat powder; so it’s
called the conditioned stimulus (CS). The response to it (again salivation) is called the
conditioned response (CR). The UR and the CR are usually similar but often not identical in
type or strength.

Initially investigators thought that classical conditioning involved simply learning that two
stimuli were contiguous–that they occurred close together in time, one after the other. Now
we think that what the animals learn is contingencies–that existence of something depends
upon existence of something else. With this in mind, it is possible to see that simply learning
that two stimuli were contiguous could often lead to behaviors that were maladaptive, with
http://michaeldmann.net/mann18.html

animals associating environmental events that had no real relationship. On the other hand,
the existence of superstitious behaviors, even in humans, suggests that this does occur.

It is tempting to think of extinction as an example of forgetting, but alas it is not. The

difference is that something new is learned during the process of extinction–the animal
learns that the CS is no longer a signal that the US is about to occur, rather it is a signal that
the US will not occur.

In operant conditioning (sometimes called trial-and-error learning), a person or animal

learns that it gets a reward if it does something. So, a pigeon learns that it gets food if it
pecks at a certain key, but not if it pecks at another. A rat learns that it can avoid getting an
electric shock if it presses a bar at a certain time. Presumably what the animal learns is that
one of its many behaviors (pecking or bar pressing) is followed by food. It is constitutional
in animals to repeat behaviors that lead to positive reinforcement (something pleasant or
the absence of something unpleasant) and avoid behaviors that lead to punishment or
negative reinforcement.

Neuroscience of Learning and Memory

A great deal has been written about the kinds and properties of learning. What has been
said here is probably enough for the purposes of this chapter. If you want to know more,
you can consult any good textbook on learning or the psychology of learning. We want to
know about what is going on in the brain when a person or animal learns something, stores
what has been learned and later retrieves it for use in behavior.

Explicit Memory

In overview, experiments on learning can be interpreted to say that explicit memory is first
acquired through one or more of the three polymodal association areas of the cerebral
cortex, namely prefrontal, limbic and parieto-occipital-temporal. Then, the information is
transferred to parahippocampal and perirhinal cortices, entorhinal cortex dentate gyrus,
hippocampus, subiculum and back to entorhinal, parahippocampal and perirhinal cortex.
The locations of these areas relative to one another are shown in Fig. 18-1, whereas a block
diagram of the connections is shown in Fig. 18-2.
http://michaeldmann.net/mann18.html

Fig. 18-1 - The relative positions of parts of the limbic system involved in learning and memory.
(Kandel, ER, JH Schwartz and TM Jessell (2000) Principles of Neural Science. New York: McGraw-Hill.)

Different forms of learning are affected differentially by lesions in different locations.

Damage to parahippocampal, perirhinal and entorhinal cortices produces greater deficits in
memory storage for object recognition than does hippocampal damage. Right hippocampal
damage produces greater deficits in memory for spatial representation, whereas left
hippocampal damage produces greater deficits in memory for words, objects or people. In
either case, the deficits are in formation of new, long-term memory; old memories are
spared.
http://michaeldmann.net/mann18.html

Fig. 18-2 - The relative positions of parts of the limbic system involved in learning and memory. (Kandel, ER,
JH Schwartz and TM Jessell (2000) Principles of Neural Science. New York: McGraw-Hill.)

Current thought is that the hippocampal system does the initial steps in long-term memory
storage–different parts being more important for different kinds of memory. The results of
hippocampal machinations–presumably memories–are transferred to the association
cortex for storage.

There is no general semantic (factual) memory store; rather memories of a single event can
be stored in multiple locations. This make sense when it is recalled that a single memory has
multiple facets–each event contains sounds, smells, tastes, somatosensory experiences,
visual images and so forth. Long-term storage of episodic (event) memories seems to occur
in prefrontal association cortex.

So, each new explicit memory is formed by four sequential processes:

Encoding-information for each memory is assembled from the different sensory

systems and translated into whatever form necessary to be remembered. This is
presumably the domain of the association cortices and perhaps other areas.

Consolidation-converting the encoded information into a form that can be

permanently stored. The hippocampal and surrounding areas apparently accomplish
this.
http://michaeldmann.net/mann18.html

Storage-the actual deposition of the memories into the final resting places–this is
though to be in association cortex.

Retrieval-memories are of little use if they cannot be read out for later use. Less is
known about this process.

Implicit Memory

Implicit memories are stored differently depending upon how they are acquired. “Fear
conditioning” (training that involves use of fearful stimuli) involves the amygdala. Operant
conditioning involves the striatum and cerebellum. For example, eye blink conditioning is
disrupted by lesions of the dentate and interpositus nuclei of the cerebellum. Classical
conditioning, sensitization and habituation involve the sensory and motor systems involved
in producing the motor responses being conditioned. Perhaps surprisingly, certain simple
reflexes mediated by the spinal cord can be classically conditioned even after the cord has
been surgically isolated from the brain. So, it appears that all regions of the nervous system
may be capable of memory storage.

Processes of Learning

Given the definitions for learning and memory, what sort of

mechanisms would we expect to find in the nervous system? One early
thought was that neurons in “memory” pathways were arranged in
reverberating circuits. In such a circuit, one neuron excites another and
the other excites the one such that, once the circuit is activated, action
potentials run around continuously. An example of this kind of Fig. 18-3 - A
reverberating
arrangement is shown in Fig. 18-3. Here are shown only 2 neurons in
circuit: Neuron A
the circuit but any number may be included. If this kind of arrangement excites B and vice
accounts for memory, then any event that temporarily stopped activity versa. (Kandel, ER,
in the circuit should disrupt memory. Unfortunately for supporters of JH Schwartz and TM
the idea, electroconvulsive shock, which temporarily stops or resets all Jessell
(2000)Principles of
electrical activity in the nervous system produces only a significant,
Neural Science. New
transitory loss of recent memory, but no loss of older memories. York: McGraw-Hill.)

Some years ago, the psychologist Donald Hebb (Hebb, DO (1949) The
Organization of Behavior: A Neuropsychological Theory. New York: John Wiley) mulled this
problem and came up with a principle that has become known as Hebb’s rule. Briefly, the
principle is “When an axon of cell A . . . excites cell B and repeatedly or persistently takes
part in firing it, some growth process or metabolic change takes place in one or both cells
http://michaeldmann.net/mann18.html

so that A’s efficiency as one of the cells firing B is increased.” As we shall see, current
thought is an extension of Hebb’s rule.

Habituation

What happens in
the nervous system
to produce
habituation?
Experiments
performed
in Aplysia
californica, the sea
slug, were designed
to address this
problem. Their
results are shown
schematically in Fig.
18-4. If the siphon
of the animal is
stimulated
mechanically the
animal withdraws
the gill, presumably
for protection. That
action is known to
occur because the
stimulus activates
receptors in the
siphon, which
activates, directly
or indirectly Fig. 18-4 - Simplified neural circuits involved in the habituation process inAplysia.
through an There are about 24 sensory neurons in the siphon; these are glutaminergic. They
interneuron, the synapse on 6 motor neurons that innervate the gill and various interneurons as
motoneuron that shown. The control condition is shown on the left, the habituated condition on the
withdraws the gill. right. (Kandel, ER, JH Schwartz and TM Jessell (2000) Principles of Neural Science.
New York: McGraw-Hill.)
This is a simple
reflex circuit. All of
this is shown on the left side of the figure. With repeated activation, the stimulus leads to a
decrease in the number of dopamine-containing vesicles that release their contents onto
the motoneuron. There appears to be no change in the sensitivity of postsynaptic NMDA or
http://michaeldmann.net/mann18.html

non-NMDA receptors. As yet, we don’t know why the dopamine release decreases. It is
presumed that habituation in vertebrates, including man, occurs by a similar process.

Sensitization

In sensitization, a stimulus to one pathway enhances reflex strength in another. An example,

again taken from experiments in Aplysia, is shown in Fig. 18-5. Again, stimulation of the
siphon leads the animal to withdraw the gill by activating sensory neuron 1, which in turn
activates a motoneuron. If the tail of the animal is stimulated just before the siphon is, then
the withdrawal of the gill is quicker and more forceful. The mechanism of this appears to
involve serotoninergic, axo-axonic synapses. As shown in the figure, activation of the
sensory receptors in the tail activates, through sensory neuron 2, a facilitating interneuron
that excites sensory neuron 1 in the pathway leading the gill withdrawal. It does this either
at the cell body or at the terminals of the sensory neuron on the motoneuron or the
interneuron. The consequence of the sensitization process is to increase the size of the EPSP
in the motoneuron without increasing the response of sensory neuron 1. This will cause a
greater response in the motoneuron and therefore a greater withdrawal of the gill.
http://michaeldmann.net/mann18.html

Fig. 18-5 - Sensitization is produced by applying a noxious stimulus to the tail of the Aplysia's tail, activated
sensory neuron 2. This, in turn activates a facilitating interneuron that enhances transmission in the pathway
from the siphon to the motor neuron. (Kandel, ER, JH Schwartz and TM Jessell (2000)Principles of Neural
Science. New York: McGraw-Hill.)

How all this occurs is illustrated in Fig. 18-6, which shows an axo-axonic synapse as might
occur between the facilitating interneuron and sensory neuron 1. Serotonin (5-
hydroxytryptamine or 5HT) is released by the presynaptic axon onto the postsynaptic axon
where it binds to receptors and activates a G protein that, in turn, activates adenylyl cyclase
to produce cAMP. This cAMP activates a cAMP-dependent protein kinase, PKA. Along with
another kinase, PKC, PKA phosphorylates and closes K channels (hypopolarizing the cell),
mobilizes vesicles for exocytosis and opens Ca channels. The end result is that activation of
this 5HT pathway by tail stimulation causes more transmitter substance to be released by
siphon stimulation, the resulting larger EPSP leads to a larger response by the gill.
http://michaeldmann.net/mann18.html

With only short-

term tail
stimulation, the
sensitization will
fairly quickly
disappear when
tail stimulation
ceases. However,
the sensitization
can be made
relatively
permanent by
repeated tail
stimulation. This
long-term
sensitization (and
also long-term
habituation)
occurs because
there are
structural changes
that occur in the
presynaptic
terminals (sensory
Fig. 18-6 - The synaptic and chemical events underlying presynaptic facilitation neuron 1, for
involved in producing sensitization. See text for details. (Kandel, ER, JH Schwartz example). With
and TM Jessell (2000) Principles of Neural Science. New York: McGraw-Hill.) sensitization, there
is an up to 2-fold
increase in the number of synaptic terminals in both sensory and motoneurons.
Alternatively, with habituation, there is a one-third reduction in the number of synaptic
terminals. Both of these changes require altered protein synthesis by mechanisms shown in
Fig. 18-7.
http://michaeldmann.net/mann18.html

Long-term
Potentiation

As previously detailed,
the hippocampus is
important in storage of
declarative memory. In
1973, a phenomenon
was described in the
hippocampus that may
account for declarative
memory. Since then the
same phenomenon has
been observed in
various other places
known to be involved in
memory storage. This
phenomenon is called
long-term potentiation
(LTP).

A high-frequency train
of stimuli applied to
fibers afferent to the
hippocampus increase
the amplitude of EPSPs
in the target neurons. Fig. 18-7 - Long-term storage of implicit memory for sensitization involves
changes shown in Fig. 18-6 plus changes in protein synthesis that result in
The increase lasts for formation of new synaptic connections. (Kandel, ER, JH Schwartz and TM
days or weeks and Jessell (2000) Principles of Neural Science. New York: McGraw-Hill.)
requires activation of
several afferent axons together. This property has been termed cooperativity, and it results
from the requirement of NMDA receptors that glutamate bind to them and the cell be
hypopolarized, the binding opens the channel and the hypopolarization displaces Mg++ that
blocks the channel lumen. Also required is that the pre- and postsynaptic cells both be active
at the same time. This latter property has been termed associativity. The astute student will
see that this is precisely the condition that Hebb’s law says should exist.
http://michaeldmann.net/mann18.html

The experimental setup for

demonstrating LTP is shown in Fig. 18-
8A. Recordings are made intracellularly
from CA1 neurons of the hippocampus
while stimulation is applied to the
Schaffer collaterals of CA3 neurons. The
amplitudes of the EPSPs in the CA1
neurons are shown in B. For a single
stimulus, the amplitude of the EPSPs is
plotted at 100%. When a train of stimuli
is applied instead, the amplitude of the
EPSPs augment to about 150%, whereas
with 4 such trains the amplitude
increases to 250%. Many people think
that long-term potentiation is an
example of Hebb’s rule at work and that
it is the physiological basis of memory.

During normal synaptic transmission

(Fig. 18-9), glutamate binds to non-
Fig. 18-8 - A. Experimental setup for demon-strating LTP
NMDA receptors allowing cations to flow in the hippocampus. The Schaffer collateral pathway is
through the channels and the cell stimulated to cause a response in pyramidal cells of CA1.
membrane to hypopolarize. Glutamate B. Comparison of EPSP size in early and late LTP with the
also binds to metabotropic receptors, early phase evoked by a single train and the late phase
activating PLC, and to NMDA receptors. by 4 trains of pulses. (Kandel, ER, JH Schwartz and TM
Jessell (2000) Principles of Neural Science. New York:
As you may already know, NMDA McGraw-Hill.)
receptor channels can bind glutamate
but no current will flow through the
channels unless the Mg++ that binds to the channel lumen is displaced. The latter event can
be effected by hypopolarizing the cell.
http://michaeldmann.net/mann18.html

Fig. 18-9 - During normal low-frequency trans-mission, glutamate interacts with NMDA and non-NMDA
(AMPA) and metabotropic receptors. (Kandel, ER, JH Schwartz and TM Jessell (2000) Principles of Neural
Science. New York: McGraw-Hill.)

By contrast, during the early phase of LTP, the high-frequency stimulation opens non-NMDA
glutamate channels leading to hypopolarization. This dislodges Mg++ from the NMDA
glutamate channels, and Ca++ enters the cells. The calcium triggers the activity of Ca-
dependent kinases, PKC and Ca-calmodulin, and tyrosine kinase. Ca-calmodulin kinase
phosphorylates non-NMDA channels, increasing their sensitivity to glutamate and a
messenger is sent retrogradely to the presynaptic terminal to increase the release of
transmitter substance. All of this is illustrated in Fig. 18-10. These events increase the
transmitter released by presynaptic terminals. With LTP, there is a decrease in transmission
failure, i.e., synapses are more reliable in exciting postsynaptic cells. This is also shown in
the figure.
http://michaeldmann.net/mann18.html

Fig. 18-10 - With high-frequency stimulation other events occur as described in the text. (Kandel, ER, JH
Schwartz and TM Jessell (2000) Principles of Neural Science. New York: McGraw-Hill.)

In the late phase of LTP (Fig. 18-11), calcium enters the cell and triggers Ca-calmodulin,
which in turn activates adenylyl cyclase and cAMP kinase. The latter translates to the
nucleus of the cell and starts processes that lead to protein synthesis and to structural
changes, i.e., the formation of new synapses. Many scientists believe that this is the
substrate for long-term memory–the formation of new synapses.
http://michaeldmann.net/mann18.html

Fig. 18-11 - For LTP to last (Late LTP) the events of Fig. 18-10 must also lead to changes in protein synthesis
and to formation of new synaptic connections. (Kandel, ER, JH Schwartz and TM Jessell (2000) Principles of
Neural Science. New York: McGraw-Hill.)
http://michaeldmann.net/mann18.html

There are still unanswered questions about the relationship of LTP to memory. First,
memories last decades whereas LTP has been observed only for days or weeks. How long
LTP can be maintained is difficult to determine. Admittedly, LTP is the longest lasting process
known in neuroscience. Still memories may last much longer. LTP occurs in most or all of
the places where memories are known to be stored. What is not known is whether
disruption of LTP also interferes with memory.

Summary
Non-declarative (implicit) memory involves different brain regions: fear conditioning
involves amygdala; operant conditioning involves striatum and cerebellum; and classical
conditioning, sensitization and habituation involve sensory and motor systems used in the
responses. This kind of memory involves a number of processes: habituation involves
decrease in synaptic strength from decreased transmitter release; sensitization involves
increase in synaptic strength due to presynaptic facilitation; and classical conditioning
involves increase in synaptic strength due to presynaptic facilitation that is dependent on
activity in both pre- and postsynaptic cells.

Declarative (explicit) memory also involves a number of brain regions: there is no general
store for explicit memories; because the subject of memories is multimodal, storage of
different aspects occurs in different locations; the hippocampal formation is important in
processing information for storage as memory; and memories are actually stored in
association cortex. This kind of memory probably makes use of long-term potentiation. The
early phase of LTP involves glutamatergic transmission; postsynaptic processes that
produce enhanced sensitivity or receptors to glutamate as well as enhanced release of
transmitter substance. In the late phase of LTP, protein synthesis leads to changes in cell
structure and formation of new synapses.

Suggested Reading
 Dudai, Y (1989) The Neurobiology of Memory: Concepts, Findings, Trends. Oxford:
Oxford University Press.
 Hebb, DO (1949) The Organization of Behavior: A Neuropsychological Theory. New
York: John Wiley
 Hull, CL (1943) Principles of Behavior. New York: Appleton-Century-Crofts.
 Kandel, ER, JH Schwartz and TM Jessell (2000) Principles of Neural Science. New
York: McGraw-Hill.
 Kandel, ER and JH Schwartz (1982) Molecular biology of learning: Modulation of
transmitter release. Science 218:433-443
http://michaeldmann.net/mann18.html

 Kimble, GA (1961) Hilgard and Marquis’ Conditioning and Learning. 2nd Edition. New
York: Appleton-Century-Crofts.
 Nicoll, RA, JA Kauer and RC Malenka (1988) The current excitement in long-term
potentiation. Neuron 1:97-103.
 Sargent, SS and KR Stafford (1965) Basic Teachings of the Great Psychologists.
Garden City, NY: Dolphin Books.

[TOC] [Chapter 19][Glossary] [Index] [Abbreviations]

This page was updated: 07/21/2011 02:02:48