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PowerPoint Presentation for
Biopsychology, 8th Edition
by John P.J. Pinel
Prepared by Jeffrey W. Grimm
Western Washington University
Copyright © 2011 Pearson Education,
Inc. All rights reserved.
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Chapter 11
Learning, Memory, and Amnesia
How Your Brain Stores
Information
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Amnesic Effects of Bilateral
Medial Temporal Lobectomy


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H.M. – an epileptic who had his temporal
lobes removed in 1953
His seizures were dramatically reduced
but so was his long-term memory
Mild retrograde amnesia and severe
anterograde amnesia
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FIGURE 11.1 Medial temporal lobectomy.
The portions of the medial temporal
lobes that were removed from H.M.’s
brain are illustrated in a view of the
inferior surface of the brain.
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Amnesic Effects of Bilateral
Medial Temporal Lobectomy
Continued

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Retrograde (backward-acting) – unable to
remember the past
Anterograde (forward-acting) – unable to
form new memories
While H.M. is unable to form most types of
new long-term memories (LTM), his shortterm memory (STM) is intact
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Formal Assessment of H.M.’s
Anterograde Amnesia:
Discovery of Unconscious
Memories


Digit span – H.M. can repeat digits
provided the time between learning and
recall is within the duration of STM
Block-tapping memory-span test – this test
demonstrated that H.M.s’ amnesia was
global – not limited to one sensory
modality
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Assessing H.M. Continued


H.M. improves with practice on
sensorimotor tasks (mirror-drawing,
rotary-pursuit) and on a nonsensorimotor
task (incomplete-pictures) – without
recalling previous practice sessions
H.M. readily “learns” responses through
classical (Pavlovian) conditioning, but has
no memory of conditioning trials
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Three Major Scientific
Contributions of H.M.’s Case


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Medial temporal lobes are involved in
memory
STM, remote memory, and LTM are
distinctly separate – H.M. is unable to move
memories from STM to LTM, a problem with
memory consolidation
Memory may exist but not be recalled – as
when H.M. exhibits a skill he does not know
he has learned (explicit vs. implicit
memories)
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Explicit vs. Implicit Memories

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Explicit memories: conscious memories
Implicit memories: unconscious memories,
as when H.M. shows the benefits of prior
experience
Repetition priming tests: used to assess
implicit memory; performance in identifying
word fragments is improved when the words
have been seen before
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FIGURE 11.4 Two items from the
incomplete-pictures test.
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Medial Temporal Lobe
Amnesia

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
Not all patients with this form of amnesia
are unable to form new explicit long-term
memories
Semantic memory (general information)
may function normally while episodic
memory (events that one has experienced)
does not
Medial temporal lobe amnesiacs may have
trouble imagining future events
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Effects of Cerebral Ischemia
on the Hippocampus and
Memory
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R.B. suffered damage to just one part of the
hippocampus (CA1 pyramidal cell layer)
and developed amnesia
R.B.’s case suggests that hippocampal
damage alone can produce amnesia
H.M.’s damage and amnesia were more
severe than R.B.’s
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FIGURE 11.5 The major components
of the hippocampus: CA1, CA2, CA3,
and CA4 subfields and the dentate
gyrus.
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Amnesia of Korsakoff’s
Syndrome
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Most commonly seen in severe alcoholics
(or others with a thiamine deficiency)
Characterized by amnesia, confusion,
personality changes, and physical
problems
Damage in the medial diencephalon:
medial thalamus + medial hypothalamus
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Amnesia of Korsakoff’s
Syndrome Continued

Amnesia comparable to medial temporal
lobe amnesia in the early stages


Differs in later stages
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Anterograde amnesia for episodic memories
Severe retrograde amnesia develops
Differs in that it is progressive,
complicating its study
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What Damage Causes the
Amnesia Seen in Korsakoff’s?

Hypothalamic mammillary bodies?
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
Thalamic mediodorsal nuclei?
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No: Korsakoff’s amnesia is seen in cases
without such damage
Possibly: damage is seen here when there is
no mammillary bodies damage
Cause of amnesia is not likely to be
damage to a single diencephalic structure
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Amnesia of Alzheimer’s
Disease (AD)
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Begins with slight loss of memory and
progresses to dementia
General deficits in predementia AD

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Major anterograde and retrograde amnesia in
explicit memory tests
Deficits in STM and some types of implicit
memory – verbal and perceptual
Implicit sensorimotor memory is intact
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What Damage Causes the
Amnesia Seen in AD?

Decreased acetylcholine

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Due to basal forebrain degeneration
Basal forebrain strokes can cause amnesia
and attentional deficits, which may be
mistaken for memory deficits
Medial temporal lobe and prefrontal cortex
also involved
Damage is diffuse

resulting amnesia is likely a consequence of
acetylcholine depletion and brain damage
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Amnesia after Concussion:
Evidence for Consolidation
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Posttraumatic amnesia: concussions may
cause retrograde amnesia for the period
before the blow and some anterograde
amnesia after
The same is seen with comas, with the
severity of the amnesia correlated with the
duration of the coma
Period of anterograde amnesia suggests a
temporary failure of memory consolidation
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Gradients of Retrograde
Amnesia and Memory
Consolidation
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Concussions disrupt consolidation (storage) of recent
memories
Hebb’s theory – memories are stored in the short term
by neural activity
Interference with this activity prevents memory
consolidation. Examples:
 Blows to the head (i.e., concussion)
 ECS (electronconvulsive shock)
Long gradients of retrograde amnesia are
inconsistent with consolidation theory
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The Hippocampus and
Consolidation

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H.M. has some retrograde amnesia
Perhaps the hippocampus stores
memories temporarily (standard
consolidation theory)


Consistent with the temporally graded
retrograde amnesia seen in experimental
animals with temporal lobe lesions
Or, perhaps the hippocampus stores
memories permanently, but they become
“stronger” over time
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Reconsolidation
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Each time a memory is retrieved from LTM,
it is temporarily held in STM
Memory in STM is susceptible to posttraumatic amnesia until it is
reconsolidated
Anisomycin, a protein synthesis inhibitor,
prevents reconsolidation of conditioned
fear in rats if applied directly to the
amygdalae
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Neuroanatomy of ObjectRecognition Memory

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Early animal models of amnesia involved
implicit memory and assumed the
hippocampus was key
1970s – monkeys with bilateral medial
temporal lobectomies show LTM deficits in
explicit memory, the delayed nonmatchingto-sample test
Like H.M., performance was normal when
memory needed to be held for only a few
seconds (within the duration of STM)
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FIGURE 11.9 The correct performance
of a delayed nonmatching-to-sample
trial. (Based on Mishkin &
Appenzeller, 1987.)
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Delayed Nonmatching-toSample Test for Rats

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Aspiration used to lesion the hippocampus
in monkeys – resulting in additional cortical
damage
Extraneous damage is limited in rats due
to lesion methods used
Bilateral damage to rat hippocampus,
amygdala, and rhinal cortex produces the
same deficits seen in monkeys with
hippocampal lesions
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Neuroanatomical Basis of the
Object-Recognition Deficits
Resulting from Medial Temporal
Lobectomy
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Bilateral removal of the rhinal cortex
consistently results in object-recognition deficits
Bilateral removal of the hippocampus produces
no or moderate effects on object recognition
Bilateral removal of the amygdala has no effect
on object recognition
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FIGURE 11.11 The three major
structures of the medial temporal
lobe, illustrated in the monkey brain:
the hippocampus, the amygdala, and
the rhinal cortex.
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A Paradox


Complete removal of the hippocampus
results in a moderate deficit in object
recognition, but small lesions of the
hippocampus (from ischemias) lead to a
severe deficit
How can this be?
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A Hypothesis

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Ischemia-induced hyperactivity of CA1
pyramidal cells damages neurons outside of
the hippocampus
Extrahippocampal damage is not readily
detectable
Extrahippocampal damage is largely
responsible for ischemia-induced object
recognition deficits
Evidence?
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A Hypothesis Continued

Ischemia-induced hyperactivity leads to
extrahippocampal damage that explains
ischemia-induced object recognition
deficits


Bilateral hippocampectomy prevents
ischemia-induced deficits
Also supported by functional brain-imaging
studies
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Hippocampus and Memory for
Spatial Location
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Rhinal cortex plays an important role in object
recognition
Hippocampus plays a key role in memory for spatial
location
 Hippocampectomy produces deficits on Morris maze
and radial arm maze
Many hippocampal cells are place cells, responding
when a subject is in a particular place and to other
cues
 Grid cells also found in hippocampus and entorhinal
cortex
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Comparative Studies of the
Hippocampus



Food-caching birds: caching and retrieving
is needed for hippocampal growth
Primate studies are inconsistent: no place
cells
Perhaps discrepancies due to different
testing paradigms (navigating the
environment vs. locating on a computer
screen)
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Theories of Hippocampal
Function


Cognitive map theory: hippocampus constructs and
stores allocentric maps of the world
Theory has been challenged
 Firing of place cells sometimes depends on other
behaviors
 Hippocampal damage sometimes impairs
behavior without a spatial component
 The hippocampus is large and complex and its
component substructures need to be evaluated in
more detail
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Where Are Memories Stored?


Each memory is stored diffusely throughout
the brain structures that were involved in its
formation
Some structures have particular roles in
storage of memories

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Hippocampus – spatial location
Perirhinal cortex – object recognition
Mediodorsal nucleus – Korsakoff’s symptoms
Basal forebrain – Alzheimer’s symptomos
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Where Are Memories Stored?
Continued


Damage to a variety of structures results
in memory deficits
Inferotemporal cortex
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Visual perception of objects
Changes in activity seen with visual recall
Amygdala


Emotional learning
Lesions of the amygdalae disrupt fear learning
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Where Are Memories Stored?
Continued

Prefrontal cortex

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Temporal order of events and working memory
Tasks involving a series of responses
Different part of prefrontal cortex may mediate
different types of working memory

Some evidence from functional brain imaging
studies
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Where Are Memories Stored?
Continued

Cerebellum and striatum

Cerebellum


Stores memories of sensorimotor skills
Striatum

Habit formation
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Synaptic Mechanisms of
Learning and Memory

Molecular events that appear to underlie
learning and memory

Hebb


Changes in synaptic efficiency are the basis of LTM
Long-term potentiation (LTP)

Synapses are effectively made stronger by repeated
stimulation
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Long-Term Potentiation (LTP)

LTP is consistent with the synaptic
changes hypothesized by Hebb

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
LTP can last for many weeks
LTP only occurs if presynaptic firing is followed
by postsynaptic firing
Hebb’s postulate for learning

Co-occurrence of firings in pre- and
postsynaptic neurons necessary for learning
and memory
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LTP as a Neural Mechanism of
Learning and Memory

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Elicited by high frequency electrical
stimulation of presynaptic neuron; mimics
normal neural activity
LTP effects are greatest in brain areas
involved in learning and memory
Learning can produce LTP-like changes
Drugs that impact learning often have
parallel effects on LTP
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FIGURE 11.19 Long-term
potentiation in the granule cell
layer of the rat hippocampal
dentate gyrus. (Traces
courtesy of Michael Corcoran,
Department of Psychology,
University of Saskatchewan.)
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LTP as a Neural Mechanism of
Learning and Memory
Continued
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
Much indirect evidence supports a role for
LTP in learning and memory
LTP can be viewed as a three-part
process:



Induction (learning)
Maintenance (memory)
Expression (recall)
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Induction of LTP: Learning

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
Most commonly studied where NMDA
glutamate receptors are prominent
NMDA receptors do not respond maximally
unless glutamate binds and the neuron is
already partially depolarized
Ca2+ channels do not open fully unless
both conditions are met
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Induction of LTP: Learning
Continued


Ca2+ influx only occurs if there is the cooccurrence that is needed for LTP,
leading to the binding of glutamate at an
NMDA receptor that is already
depolarized
Ca2+ influx may activate protein kinases
that induces changes causing LTP
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Maintenance and Expression
of LTP: Storage and Recall
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Pre- and postsynaptic changes
LTP is only seen in synapses where it was
induced
Protein-synthesis (structural changes)
underlies long-term changes
LTP begins in the postsynaptic neuron,
which signals the presynaptic neuron
Astrocytes (not just neurons) also involved
in LTP
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Maintenance and Expression of
LTP: Storage and Recall
Continued
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

How are presynaptic and postsynaptic
changes coordinated?
Nitric oxide synthesized in postsynaptic
neurons in response to Ca2+ influx may
diffuse back to presynaptic neurons
Structural changes are now a wellestablished consequence of LTP
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Variability of LTP

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Most LTP research has focused on NMDAreceptor-mediated LTP in the
hippocampus, but LTP is mediated by
different mechanisms elsewhere
LTD (long-term depression) also exists
Much of LTP and the neural basis of
memory is still a mystery, despite many
research discoveries
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Infantile Amnesia

Explicit and implicit memory can be
demonstrated in normal, intact subjects


Skin conductance responses (implicit memory)
elicited by pictures of preschool classmates,
whether they were explicitly recognized or not
Modern incomplete-pictures test: Previously seen
pictures were recognized sooner (implicit
memory) than new pictures, whether the old
pictures were explicitly recognized or not
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Smart Drugs: Do They Work?


Smart drugs are substances thought to
improve memory
Limited research has shown that no
purported nootropic has memoryenhancing effects in normal people
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Posttraumatic Amnesia and
Episodic Memory


May occur following head trauma
Patient may have difficulty with episodic
memory


Might include amnesia for details of their
personal life
Might also include anterograde amnesia
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