POWERPOINT PRESENTATION
FOR BIOPSYCHOLOGY,
9TH EDITION
BY JOHN P.J. PINEL
P R E PA R E D B Y J E F F R E Y W. G R I M M
WESTERN WASHINGTON UNIVERSITY
COPYRIGHT © 2014 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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Learning Objectives
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LO1: Describe the case of H.M. Explain how H.M. changed our understanding of
memory.
LO2: Compare Korsakoff’s amnesia and medial temporal lobe amnesia.
LO3: Compare Alzheimer’s amnesia with medial temporal lobe amnesia.
LO4: Define anterograde and retrograde amnesia.
LO5: Retrograde amnesia provides evidence for memory consolidation. Explain.
LO6: Describe the nonmatching-to-sample model of explicit memory.
LO7: Summarize the evidence that damage to the medial temporal cortex is
largely responsible for object-recognition deficits after medial temporal
lobectomy.
LO8: Summarize evidence that the hippocampus plays a special role in memory
for location.
LO9: Discuss the various parts of the brain thought to play a role in memory
storage.
LO10: Explain LTP and discuss its properties.
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Amnesic Effects of Bilateral
Medial Temporal Lobectomy
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H.M. was an epileptic who had his
temporal lobes removed in 1953.
His seizures were dramatically reduced—
but so was his long-term memory
H.M. experienced both 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
(Con’t)
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Retrograde (backward-acting): unable to
remember the past
Anterograde (forward-acting): unable to
form new memories
While H.M. was unable to form most types
of new long-term memories (LTM), his
short-term memory (STM) was intact.
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Formal Assessment of H.M.’s
Anterograde Amnesia: Discovery
of Unconscious Memories
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Digit span: H.M. can repeat digits,
provided that 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. (Con’t)
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H.M. improved with practice on
sensorimotor tasks (mirror drawing, rotary
pursuit) and on a nonsensorimotor task
(incomplete pictures)—all without recalling
previous practice sessions.
H.M. readily learned responses through
classical (Pavlovian) conditioning, but had
no memory of the conditioning trials.
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FIGURE 11.2 The learning and retention of
the mirrordrawing task by H.M. Despite his
good retention of the task, H.M. had no
conscious recollection of having
performed it before. (Based on Milner,
1965.)
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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. was unable to
move memories from STM to LTM, a
problem with memory consolidation.
Memory may exist but not be recalled—as
when H.M. exhibited a skill he did not know
he had 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. showed 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 11.3 Two items from the incomplete-pictures test. H.M.’s memory for
the 20 items on the test was indicated by his ability to recognize the more
fragmented versions of them when he was retested. Nevertheless, he had no
conscious awareness of having previously seen the items.
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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 11.4 The major components of the
hippocampus: CA1, CA2, CA3, and CA4
subfields and the dentate gyrus. R.B.’s
brain damage appeared to be restricted
largely to the pyramidal cell layer of the
CA1 subfield. (CA stands for cornu
ammonis, another name for hippocampus.)
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Amnesia of Korsakoff’s
Syndrome
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Korsakoff’s syndrome is most commonly
seen in severe alcoholics (or others with a
thiamine deficiency).
It is 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 (Con’t)
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Amnesia experienced by Korsakoff’s
sufferers is comparable to medial
temporal lobe amnesia in the early
stages.
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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?
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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.
The 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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AD 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?
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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.
The medial temporal lobe and prefrontal
cortex are also involved.
Damage is diffuse.
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The 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.
The 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 is that memories are stored
in the short term by neural activity.
Interference with this activity prevents
memory consolidation. Examples:
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Blows to the head (i.e., concussion)
ECS (electronconvulsive shock)
Long gradients of retrograde amnesia are
inconsistent with consolidation theory.
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FIGURE 11.5 The retrograde amnesia and
anterograde amnesia associated with a
concussion-producing blow to the head.
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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).
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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.
Not all kinds of memories are subject to
reconsolidation.
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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.
In the 1970s, monkeys with bilateral medial
temporal lobectomies showed LTM deficits in
explicit memory: the delayed nonmatching-tosample test.
As with 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 11.7 Performance of a
delayed nonmatching-to-sample trial.
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Delayed Nonmatching-toSample Test for Rats
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Aspiration is used to lesion the
hippocampus in monkeys, resulting in
additional cortical damage.
Extraneous damage is limited in rats due
to the 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 11.9 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
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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 (Con’t)
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Ischemia-induced hyperactivity leads to
extrahippocampal damage that explains
ischemia-induced object-recognition
deficits.
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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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The rhinal cortex plays an important role in object
recognition.
The hippocampus plays a key role in memory for
spatial location.
 Hippocampectomy produces deficits in Morris maze
and radial arm maze performance.
Many hippocampal cells are place cells, responding
when a subject is in a particular place (and to other
cues).
 Grid cells are also found in hippocampus and the
entorhinal cortex.
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Comparative Studies of the
Hippocampus
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Food-caching birds: caching and retrieving
is needed for hippocampal growth.
Primate studies are inconsistent; place cells
and grid cells are less prevalent.
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Place cells respond to where the subject is
looking rather than where the subject is located.
Perhaps discrepancies are due to different
testing paradigms (navigating the
environment vs. locating on a computer
screen).
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Theories of Hippocampal
Function
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Cognitive map theory: the hippocampus constructs
and stores allocentric maps of the world.
This theory has been challenged.
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The firing of place cells sometimes depends on other
behaviors.
Hippocampal damage sometimes impairs behavior
without a spatial component.
Evidence for “concept” cells in human temporal lobe
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Respond to particular individuals or related individuals (e.g.,
Jennifer Aniston but also Lisa Kudrow)
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?
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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 symptoms
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Where Are Memories Stored?
(Con’t)
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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
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Emotional learning
Lesions of the amygdalae disrupt fear learning.
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Where Are Memories Stored?
(Con’t)
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Prefrontal Cortex
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Temporal order of events and working memory
Tasks involving a series of responses
Different parts of the prefrontal cortex may
mediate different types of working memory.
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Some evidence from functional brain imaging
studies
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Where Are Memories Stored?
(Con’t)
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Cerebellum and Striatum
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Cerebellum
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Stores memories of sensorimotor skills
Striatum
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Habit formation
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FIGURE 11.16 The structures of the brain
that have been shown to play a role in memory.
Because it would have blocked the view of other
structures, the striatum is not included. (See
FIGURE 3.28 on page 71.)
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Synaptic Mechanisms of
Learning and Memory
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Molecular Events that Appear to Underlie
Learning and Memory
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Hebb
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Changes in synaptic efficiency are the basis of LTM.
Long-term potentiation (LTP)
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Synapses are effectively made stronger by repeated
stimulation.
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Long-Term Potentiation (LTP)
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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
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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 11.18 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 (Con’t)
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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.
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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
(Con’t)
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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 induce changes, causing LTP.
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FIGURE 11.19 The induction of
NMDA-receptor–mediated 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) are also
involved in LTP.
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Maintenance and Expression of
LTP: Storage and Recall (Con’t)
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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
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Explicit and implicit memory can be
demonstrated in normal, intact subjects.
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Skin conductance responses (implicit memory)
were 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?
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Smart drugs (nootropics) 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
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May Occur Following Head Trauma
Patients may have difficulty with episodic
memory.
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Might include amnesia for details of their
personal lives
Might also include anterograde amnesia
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