Transcript Learning, memory & amnesia Chapter 11

Learning, memory & amnesia
Chapter 11
The case of H.M.

Intractable epilepsy
one generalized convulsion each week
 Several partial convulsions each day


1953 surgery: Bilateral medial temporal
lobectomy
temporal pole
 amygdala
 entorhinal cortex
 hippocampus

Corkin et al. (1997)
Corkin et al. (1997)
Effects of Bilateral Medial Temporal
Lobectomy
Convulsions were dramatically reduced
 IQ increased from 104 to 118
 Short-term memory (STM) intact
 Temporally-graded retrograde amnesia
 Severe anterograde amnesia

Amnesia
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, his STM was
intact

Mirror-drawing task
H.M.’s performance
improved over 3
days (10 trials/day)
despite the fact
that he could not
consciously
remember the task
on days 2 and 3.
Rotary-Pursuit Test
H.M.’s performance
improved over 9
daily practice
sessions; again,
with no recognition
of the experience
Explicit vs Implicit Memories

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Explicit memories – conscious memories
Implicit memories – unconscious memories
Repetition priming tests were developed to assess
implicit memory performance;
Incomplete pictures test
Implications of H.M.’s amnesia
Medial temporal lobes are involved in
memory formation.
 STM and LTM are dissociable – H.M. is
unable to consolidate certain kinds of
explicit memory.
 the fact that he could form some memories
suggests that there are multiple memory
systems in the brain.

Medial Temporal Lobe Amnesia

Not all patients with this form of amnesia are
unable form new explicit long-term memories, as
was the case with H.M.
Two kinds of explicit memory:
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)
Vargha-Khadem et al., (1997)
Studied three children that had bilateral
temporal lobe damage early in life.
 Like H.M., the children could not form
episodic memory, however they did
acquire reasonable levels of factual
knowledge and language ability in
mainstream school.

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

Object-Recognition Memory
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Early animal models of amnesia involved implicit
memory and assumed the hippocampus was
key
1970’s – monkeys with bilateral medial temporal
lobectomies showed 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)
Delayed nonmatching-to-sample task
pretend you’re the monkey
Sample stimulus
touch it and get a yummy treat
10 min delay during which other
sample stimuli are presented
Choice phase: pick the image that is new
Darn, no food
Another
yummy treat
Testing object-recognition memory
Medial temporal lobe (MTL)
Delayed non-match to sample results
The Mumby Box
Object recognition in rats
Comparison
of lesions in
monkeys
and rats
Neuroanatomy of object recognition
Bilateral removal of the rhinal cortex
consistently results in object-recognition
deficits.
 Bilateral removal of the hippocampus
produces moderate deficits or none at all.
 Bilateral removal of the amygdala has no
effect on object-recognition.

Is the hippocampus involved in
object recognition memory?
The Case of R.B. suggests that the lesions
of the CA1 region of the hippocampus
(due to ischemia) can produce severe
memory deficits
 Ischemia in animal models also produces
deficits in object recognition
 Yet deficits in object recognition are only
moderate to non-existent in other animal
lesion models
 Why?

Mumby et al. (1996)
Bilateral hippocampectomy actually blocks
the damage produced by ischemia!
Explanation:
 Ischemia causes hippocampal neurons to
release glutamate, which produces
damage outside of the hippocampus
(particularly in rhinal cortex), although
standard histological techniques do not
show the damage follow-up functional
imaging studies have confirmed the
dysfunction.

The Hippocampus
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
(Chapter 5)
 Many hippocampal cells are place cells –
responding when a subject is in a
particular place

Theories of Hippocampal Function
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O’Keefe & Nadel (1978) Cognitive map theory –
constructs and stores allocentric maps of the
world
Rudy & Sutherland (1992) Configural
association theory – involved in retaining the
behavioral significance of combinations of
stimuli
Brown & Aggleton (1999) is involved in
recognizing the spatial arrangements of objects
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 LTM
 Long-term potentiation (LTP) – synapses
are effectively made stronger by repeated
stimulation

Long Term Potentiation (LTP)
Cross-section of the NMDA receptor complex
Ca2+
NMDA
Glutamate
+
AP-5
Na
D-Cycloserine
Glycine
Polyamine
HA-966
Zn 2+
PCP
Mg
MK-801
2+
Mg 2+
K+