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Copyright © 2007 by Allyn and Bacon
Chapter 9Learning, Memory, and AmnesiaHow Your Brain Stores Information
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Copyright © 2007 by Allyn and Bacon
The Brain Changes its Functioning in Response to Experience Learning –how experience changes the
brain Memory –how changes are stored and
subsequently reactivated What brain structures are involved in
processes of learning and memory?
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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 memory
Mild retrograde amnesia and severe anterograde amnesia
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Amnesia
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, his STM is intact
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Assessing H.M.
Digit span – H.M. can repeat digits as long as the time between learning and recall is within the limits of short-term storage
Mirror-drawing task – H.M. exhibits improvement with practice. He is able to show skill memory – demonstrating that he can learn some things (also rotary-pursuit and a drawing task) – although he is not aware of it
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Assessing H.M.
H.M. readily “learns” responses through Pavlovian (classical) conditioning
H.M. can learn some things, but has no memory of having learned them
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Scientific Contributions of H.M.’s Case Medial temporal lobes are involved in
memory Short-term memory (STM) and long-term
memory (LTM) are distinctly separate H.M. is unable to move memories from
STM to LTM, a problem with memory consolidation
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Scientific Contributions of H.M.’s Case Memory may exist but not be recalled –
as when H.M. exhibits a skill he does not know he has learned
H.M. forms new implicit memories, but not new explicit memories
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Explicit Vs Implicit Memories
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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Medial Temporal Lobe Amnesia
Not all with this form of amnesia are unable form new explicit long-term memories – as was the case with H.M.
Semantic memory (general information) may function normally while episodic memory (events that one has experienced) does not – they are able to learn facts, but do not remember doing so (the episode when it occurred)
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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 – was more severe than R.B.’s
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Korsakoff’s Syndrome
Most commonly seen in who? Alcoholics Also seen in individuals with a
thiamine-deficient diet Alcohol causes a disruption in the
body’s ability to use thiamine
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Korsakoff’s Syndrome
Characterized by amnesia, confusion, personality changes, and physical problems
Typically damage in the medial diencephalon – medial thalamus + medial hypothalamus
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Korsakoff’s Syndrome
Amnesia comparable to medial temporal lobe amnesia in the early stagesAnterograde amnesia for episodic memories
Differs in later stagesSevere 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?
No – Korsakoff’s amnesia is seen in cases without such damage
Thalamic mediodorsal nuclei?Possibly – damage is seen here when there is
no mammillary damage Cause is not likely to be damage to a
single diencephalic structure
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Alzheimer’s Disease (AD)
Begins with slight loss of memory and progresses to dementia
General deficits in predementia ADMajor anterograde and retrograde amnesia in
explicit memory testsDeficits 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
Due to basal forebrain degeneration Basal forebrain strokes can cause amnesia and
attention 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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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 – memories are stored in the short
term by neural activity Interference with this activity prevents
memory consolidationBlows to the head (i.e., concussion)ECS (electroconvulsive shock)
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The Hippocampus and Consolidation What role does the hippocampus play in
consolidation? Some have proposed that memory storage
structures store memories for as long as they exist and eventually an engram forms
Engram – a change in the brain that stores a memory
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Object-Recognition Memory
Early animal models of amnesia involved implicit memory and assumed the hippocampus was key
1970’s – monkeys with bilateral medial temporal lobectomies show LTM deficits in 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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Testing object-recognition memory
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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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Object-Recognition Deficits and Medial Temporal Lobectomy Neuroanatomical basis of resulting deficits? Bilateral removal of the rhinal cortex > object-
recognition deficits Bilateral removal of the hippocampus > no or
moderate effects on object recognition Bilateral removal of the amygdala?
No effect on object-recognition.
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A Paradox
Removing the hippocampus has a moderate effect on object recognition while ischemia-induced lesions to a small part of it leads to severe deficits
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 not readily detectable
Extrahippocampal damage is largely responsible for ischemia-induced object recognition deficits.
Evidence?
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A Hypothesis
Ischemia-induced hyperactivity leads to extrahippocampal damage that explains ischemia-induced object recognition deficitsBilateral hippocampectomy prevents
ischemia-induced deficitsSupported by functional brain-imaging studies
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The Hippocampus
Rhinal cortex plays an important role in object recognition
Hippocampus plays a key role in memory for spatial location Hippocampal lesions producesdeficits on Morris
water and radial arm mazes Many hippocampal cells are place cells –
responding when a subject is in a particular place
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Comparative Studies of the Hippocampus Hippocampus seems to play a role in spatial
memory in many species – not just rats Food-caching birds - caching and retrieving is
needed for hippocampal growth Primate studies are inconsistent – no place cells Differences may be due to differences in testing
paradigms Navigating through the environment Vs location on a
computer screen
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Theories of Hippocampal Function
Cognitive map theory – constructs and stores allocentric maps of the world
Configural association theory – involved in retaining the behavioral significance of combinations of stimuli
Involved in recognizing spatial arrangements of objects
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Where Are Memories Stored?
Each memory is stored diffusely throughout the brain structures that were involved in its formation.
Hippocampus – spatial location Rhinal cortex – object recognition Mediodorsal nucleus – Korsakoff’s Basal forebrain – Alzheimer’s disease Damage to a variety of structures results in
memory deficits.
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Where are memories stored?
Inferotemporal cortex – visual perception of objects – changes in activity seen with visual recall
Amygdala – emotional learning – lesion leads to lack of learned fear
Prefrontal cortex – temporal order of events and working memory
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Where are memories stored?
Prefrontal cortex – damage leads to problems with tasks involving a series of responses
Different part of this structure may mediate different types of working memory – some evidence from functional brain imaging studies
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Where are memories stored?
Cerebellum and striatum – sensorimotor tasks
Cerebellum – stores memories of sensorimotor skills – conditioned eyeblink, for example
Striatum – habit formation – associations between stimuli and responses
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Synaptic Mechanisms of Learning and Memory What is happening within the brain
structures involved in memory? Hebb – changes in synaptic efficiency
are the basis of long-term memory Long-term potentiation (LTP) –
synapses are effectively made stronger by repeated stimulation
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LTP as a Neural Mechanism of Learning and Memory Consistent with the synaptic changes
hypothesized by HebbLTP can last for many weeks.LTP only occurs if presynaptic firing is
followed by postsynaptic firing Hebb’s postulate for learning
Co-occurrence is necessary for learning and memory
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LTP as a Neural Mechanism of Learning and Memory Elicited by levels of stimulation that mimic
normal neural activity LTP effects 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 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
Usually studied where NMDA glutamate receptors are prominent
NMDA receptors do not respond maximally unless glutamate binds and the neuron is already depolarized
Calcium channels do not open fully unless both conditions are met
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Induction of LTP: Learning
Calcium 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
Calcium 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 underlies long-term
changes Long-lasting changes in extracellular
glutamate levels
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Maintenance and Expression of LTP: Storage and Recall How are presynaptic and postsynaptic
changes coordinated? Nitric oxide synthesized in postsynaptic
neurons in response to calcium influx may diffuse back to presynaptic neurons
Structural changes are now a well-established consequence of LTP
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LTP – A Final Note
Most LTP research has focused on NMDA-receptor-mediated LTP in the hippocampus, but LTP is mediated by different mechanisms elsewhere.
LTD, long-term depression, also exists
Why should there be a variety of mechanisms and places that underlie learning and memory?