Transcript 2605_lect11.ppt

BIOPSYCHOLOGY 8e
John P.J. Pinel
Copyright © Pearson Education 2011
Topics
11.1 Amnesic Effects of Bilateral Medial
Temporal Lobectomy
11.2 Amnesia of Korsakoff’s Syndrome
11.3 Amnesia of Alzheimer’s Disease
11.4 Amnesia after Concussion: Evidence
for Consolidation
11.5 Neuroanatomy of Object-Recognition
Memory
11.6 Hippocampus and Memory for Spatial
Location
11.7 Where Are Memories Stored?
11.8 Synaptic Mechanisms of Learning
and Memory
11.9 Conclusion: Biopsychology of
Memory and You
Amnesic Effects of Bilateral Medial Temporal
Lobectomy
• 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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Amnesic Effects of Bilateral Medial Temporal
Lobectomy
Retrograde
• Backward-acting
• Unable to remember the
past
Anterograde
• Forward-acting
• Unable to form new
memories
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Amnesic Effects of Bilateral Medial Temporal
Lobectomy
• While H.M. is unable to
form most types of new
long-term memories
(LTM), his short-term
memory (STM) is intact
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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Formal Assessment of H.M.’s Anterograde Amnesia:
Discovery of Unconscious Memories
• H.M improves with practice on sensorimotor
• Digit span – H.M. can repeat digits provided
tasks (mirror-drawing, rotary pursuit) and on
the time between learning and recall is within
a non sensorimotor task (incompletethe duration of STM
pictures) – without recalling previous practice
• Block-tapping memory-span test – this test
sessions
demonstrated that H.M.s’ amnesia was
• H.M. Readily “learns” responses through
global – not limited to one sensory modality
classical (Pavlovian) conditioning, but has no
memory of conditioning trials
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Three Major Scientific Contributions of H.M.’s case
• 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 hen H.M. exhibits a
skill he does not know he has
learned (explicit vs. implicit)
Explicit vs. Implicit Memories
• Conscious
memories
• Unconscious
memories, as when
H.M. shows the
benefits of prior
experience
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Explicit vs. Implicit Memories
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Medial Temporal Lobe Amnesia
•Not all patients with this
form of amnesia are unable
to form new explicit longterm 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
• 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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Amnesia of Korsakoff’s Syndrome
Most commonly seen in severe
alocholics (or others with a tyiamine
deficiency)
• Characterized by amnesia, confusion,
personality changes, and physical
problems
• Damage in the medial diencephalon: medial
thalamus + medial hypothalamus
• Amnesia comparable to medial
temporal lobe amnesia in the early
stages
• Differs in later stages (it becomes
progressive, complicating its study)
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Amnesia of Alzheimer’s Disease (AD)
• Begins with slight loss of
memory and progresses to
dementia
• General deficits in
predementia AD:
• 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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Amnesia after Concussion: Evidence for Consolidation
• 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
• 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., a concussion)
• ECS (electroconvulsive shock)
• Long gradients of retrograde amnesia are
inconsistent with consolidation theory
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The Hippocampus and Consolidation
• 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
• 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 Object-Recognition Memory
• 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
nonmatching-to-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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Delayed Nonmatching-to-Sample Test for Rats
• 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
• 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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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
• 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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Hippocampus and Memory for Spatial Location
• 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
• Challenges to this theory:
• 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
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
• 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?
• Prefrontal cortex
• 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
• 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)
The human brain
• LTP is consistent with the synaptic changes
hypothesized by Hebb
• 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
The human brain
• 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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LTP as a Neural Mechanism of Learning and Memory
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
LTP can be viewed
as a three-part
process:
• Induction
(learning)
• Maintenance
(memory)
• Expression
(recall)
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Induction of LTP: Learning
• 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
• Ca2+ influx only occurs if
there is the co-occurrence
that is needed for LTP,
leading to the binding of
glutamate at an NMDA
receptor that is already
depolarized
• NMDA/AMPA story (not in
text)
• Ca2+ influx may activate
protein kinases that induces
changes causing LTP
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Maintenance and Expression of LTP: Storage and Recall
• 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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Variability of LTP
• Most LTP research has
focused on NMDA-receptormediated 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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Watch: Memory Deficit
Simulate: Memory
Simulate: Key processes in the stages
of memory
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Acknowledgments
Slide
Image Description
Image Source
template
lightning
©istockphoto.com/Soubrette
template
background texture
©istockphoto.com/Hedda Gjerpen
Ch 11 image
Woman thinking
©istockphoto.com/Cliff Parnell
3, 7, 21, 22, 25, 35
brain
©istockphoto.com/Stephen Kirklys
4
Figure 11.1
Pinel 8e, p. 269
5
counting on fingers
©istockphoto.com/Joshua Hodge Photography
9
Figure 11.4
Pinel 8e, p. 272
10
repressed memories
©istockphoto.com/Eric Hood
11
Figure 11.5
Pinel 8e, p. 275
12
green beer bottle
©istockphoto.com/Bjørn Heller
12
bottle of vitamins
©istockphoto.com/Baris Simsek
13
senior adult with hands covering face
©istockphoto.com/Duncan Walker
14
Man's head
©istockphoto.com/Nicolas Hansen
15, 26, 27
messy files
©istockphoto.com/Jelena Popic
16, 33, 34
book
©istockphoto.com/Carmen Martínez Banús
17
writing at metal table
©istockphoto.com/track5
18
Figure 11.9
Pinel 8e, p. 281
19
white rat
©iStockphoto.com/Elena Butinova
19
blue sky & clouds
©istockphoto.com/kertlis
20
Figure 11.11
Pinel 8e, p. 282
23
toddler
©istockphoto.com/Wendy Shiao
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Acknowledgments
Slide
Image Description
Image Source
24
notebook
©istockphoto.com/stockcam
24
yellow pad
©istockphoto.com/DNY59
28
woman observing & taking notes
©istockphoto.com/Claudio Arnese
29, 30
neuron
©istockphoto.com/ktsimage
31
Figure 11.19
Pinel 8e, p. 291
32
Figure 11.21
Pinel 8e, p. 293
36
person thinking
©istockphoto.com/akurtz
37
two babies
©istockphoto.com/schwester
38
pill background
©istockphoto.com/Fotografia Basica
39
man in shadow (black and white)
©istockphoto.com/blackred
40
laptop
©istockphoto.com/CostinT
40
table and wall
©istockphoto.com/David Clark
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