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Learning+and+memory

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    Learning+and+memory Learning+and+memory Presentation Transcript

    • 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).
      • -Errors (marks out of boundary) were calculated to determine learning.
      •  
      • -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).
      • 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.
      •  
      • 3. The case provided support for the view of two distinct modes of storage for STM & LTM.
      • 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!
      • - 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
    • Alzheimer’s Disease: Genetic basis???
      • -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.
      • -It may depend on at least 2 or 3 different genes
      •  
    • Alzheimer’s Disease: Neurological damage
      • 1. There is widespread atrophy of the cortex with plaques & tangles in the hippocampus.
      • 2. Entorhinal cortex is also destroyed, acetylcholine neurons are diseased.
      • 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.
      • It is thought that infants & young toddlers have early memory problems due to an immature hippocampus.
      • Older people with difficulty in explicit memory may show dying or diseased neurons in the hippocampus.
    • Evidence for hippocampus in memory:
      • 1. Case study of H.M.
      • 2. Alzheimer’s patients (often severe hippocampal damage preceeds most other damage.)
      • 3. Animal models of hippocampal damage—rats with hippocampal lesions can’t perform 8-arm 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.
      • Rats have to learn which arms have a unique cue (e.g., rough surface) that signals they have food.
      • 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.
    •  
    • Role of the frontal cortex in memory
      • The prefrontal cortex plays a large role in memory.
      • Evidence for this comes from N.A., Korsakoff’s patients, & animal models.
      • Prefrontal cortex deteriorates in older age. Aged monkeys perform more poorly on many of the same tasks as do monkeys with prefrontal cortex damage.