Transcript Learning and Memory

Learning and Memory
Dr. Kline
FSU-PC
What is memory?

What do you think???
I. STM vs. LTM

Short Term Memory (STM)-- also called working
memory is memory for events that have just occurred.
-Capacity is 5 to 7 units of information ± 2
(e.g., a phone number)

Long Term Memory (LTM) --memory for events
longer than can be held in STM & is relatively
permanent.
(e.g., Who was your first grade teacher?)
What is the process by which STM is
transferred to LTM?

What do you think???

Consolidation
Neurological & behavioral evidence that
STM & LTM exist independently of one
another:

1. People with hippocampal damage can form STM
memories, but cannot form LTM memories.

2. Head trauma victims have difficulty remembering
events just prior to the trauma, but not for memories
much earlier than the event.

3. Retrieval of information from STM is easier than for
LTM.
II. Explicit Vs. Implicit memory

Explicit memory-- memory for facts or
specific events; may be directly tested for by
asking the subject questions.
“Who is the president of the United States?”
Implicit memory --memory that does not
require specific events or facts, is largely out of
awareness & cannot be directly assessed.
(riding a bike, shifting gears in car)
III. Declarative Vs. Procedural Memory
Declarative memory --memory that a
person can state in words, is based on facts
& events.
 ---synonymous to explicit memory

Procedural memory --consists of motor
skills.
 ---similar to implicit memory (not all
implicit memory is motor)

IV. Brain Damage: Explicit Memory
impairments!
Comes from the case study of H.M (27 yrs) who
had severe epileptic seizures that were damaging
his brain.
He elected to have surgeons perform a
bilateral medial temporal lobectomy to remove
source of seizures.
Portions of the temporal lobe, hippocampus, &
and amygdala were removed.
H.M.—Post Operative

H.M.’s personality & intellect were intact.

His IQ went up a few points & seizures were
dramatically reduced.

However, he had massive memory deficits that
radically changed his life.
Memory deficits in H.M.

1. H.M. had moderate retrograde amnesia which is
loss of memory for events in the past for about a year or
two leading up to the surgery.

2. H.M.’s memory for remote events (such as events of
his childhood) was intact.

3. H.M. had profound anterograde amnesia or memory
loss for events that occurred following surgery.
--He can’t form any new Long Term memories!!!!
Formal Assessment of H.M.’s Anterograde
Amnesia:

1. Digit Span +1 Test—5 digits were read to H.M. at 1
sec. intervals. If he got all 5 correct, on the next trial the
same 5 digits were presented in the same sequence with
1 new digit added at the end & so forth for additional
trials.

-After 25 trials of this task, H.M. still could not
successfully repeat more than 7 digits (beyond STM
span).

-Most normal Ss can learn up to 18 digits!!!
2. Verbal and Nonverbal Matching to
sample tests:

The S is presented with a sample item & then after a
delay, an array of test items is presented from which the
S must select the one that matches the sample.

With verbal stimuli, H.M. did very well & could match
the items! In contrast, H.M. performed very poorly with
non-verbal stimuli.
Why????
He rehearsed the verbal material thereby keeping it in
STM, but couldn’t do this with the non-verbal stimuli.
Thus, his STM appeared to be working.

3. Mirror Drawing Test:
H.M. was to draw a line within the boundaries
of a star-shaped target by watching his hand in a
mirror (10 trials on 3 consecutive days).
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
-Errors (marks out of boundary) were calculated to
determine learning.
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-H.M. did well, showing that his implicit motor skill
learning ability was intact. However, he had no memory
for doing the task.
4. Rotary-Pursuit Test:

H.M. held a stylus in contact with a target rotating on a
revolving turntable (record player).
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He did well & improved his performance significantly
over 9 daily sessions, despite not recalling doing the task.

Again, motor skill learning had been spared or preserved.
But, explicit knowledge of having done the task was not.
The influence of H.M.’s case on search for
Neural basis of memory:

1. Was the first case to strongly implicate the medial
temporal lobes in memory (hippocampus).

2. H.M.’s case challenged the view that memorial
functions are diffusely & equivalently distributed
through the brain.
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3. The case provided support for the view of two distinct
modes of storage for STM & LTM.
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4. The medial temporal lobes play an important role in
memory consolidation.
V. Korsakoffs Syndrome:

A disease that develops in individuals who chronically
consume alcohol.

-caused by a thiamine (vitamin B 1) deficiency that
occurs almost exclusively in severe alcoholics.

-memory loss—severe retrograde & anterograde
amnesia.

neurological damage is diffuse, striking damage in
dorsal medial nucleus of thalamus, frontal cortex.
VI. The case of N.A. (1960)

N.A. was accidentally stabbed through the right nostril
with a fencing foil, that penetrated his skull & went
upwards in the forebrain.

Since the injury he had been unable to retain any new
permanent memories & has had great difficulty finding
employment.

CAT scans reveal a small lesion in the left dorsomedial
nucleus of the thalamus.
VII. Alzheimer’s Disease:

Is a progressive degenerative disease that
ultimately results in death, marked by severe
retrograde & anterograde amnesia.

Early onset: late 40’s early 50’s prior to 60’s, is
more severe that late onset!
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-Late onset: after 65, we have 50% chance of
developing this by age 85.
Alzheimer’s Disease: Symptoms
starts with minor forgetfulness (where’s
checkbook, etc.)
 Steadily progresses to serious memory loss
 Depression
 Restlessness
 Hallucinations & delusions (seeing dead
relatives)
 Anterograde & retrograde amnesia
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Alzheimer’s Disease: Genetic basis???
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-does seem to run in families, especially in
families with early onset.

-Best evidence--nearly all Down’s Syndrome
patients will eventually develop the disease if
they survive to middle age.
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-It may depend on at least 2 or 3 different genes
Alzheimer’s Disease: Neurological damage
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1. There is widespread atrophy of the cortex with
plaques & tangles in the hippocampus.
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2. Entorhinal cortex is also destroyed, acetylcholine
neurons are diseased.
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3. The plaques contain deposits of a protein known as
Beta-amyloid. An injection of this protein into a rat’s
brain can damage neurons & produce symptoms
resembling those of Alzheimer’s disease.
Role of hippocampus in memory

1. Hippocampus--It is known that the hippocampus is
critical in the consolidation of LTM.
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It is thought that infants & young toddlers have early
memory problems due to an immature hippocampus.
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Older people with difficulty in explicit memory may
show dying or diseased neurons in the hippocampus.
Evidence for hippocampus in memory:
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1. Case study of H.M.
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2. Alzheimer’s patients (often severe
hippocampal damage preceeds most other
damage.)
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3. Animal models of hippocampal damage—
rats with hippocampal lesions can’t perform 8arm radial maze task.
What is 8-arm radial maze task?

A rat is placed in the center of 8 arms of a maze in
which food is placed in the end of the arms.
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Rats have to learn which arms have a unique cue (e.g.,
rough surface) that signals they have food.
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Normal rats learn this very fast, don’t revisit arms
they’ve been to before. Rats with hippocampal
damage will reenter correct arms while failing to try
others.
In other words, they can’t remember they were there
before.
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Role of the frontal cortex in memory
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The prefrontal cortex plays a large role in memory.
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Evidence for this comes from N.A., Korsakoff’s
patients, & animal models.
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Prefrontal cortex deteriorates in older age. Aged
monkeys perform more poorly on many of the same
tasks as do monkeys with prefrontal cortex damage.