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  1. 1. Learning and Memory Dr. Kline FSU-PC
  2. 2. What is memory? <ul><li>What do you think??? </li></ul>
  3. 3. I. STM vs. LTM <ul><li>Short Term Memory (STM)-- also called working memory is memory for events that have just occurred. </li></ul><ul><li>  -Capacity is 5 to 7 units of information ± 2 </li></ul><ul><li>(e.g., a phone number) </li></ul><ul><li>Long Term Memory (LTM) --memory for events longer than can be held in STM & is relatively permanent. </li></ul><ul><li>(e.g., Who was your first grade teacher?) </li></ul>
  4. 4. What is the process by which STM is transferred to LTM? <ul><li>What do you think??? </li></ul><ul><li>Consolidation </li></ul>
  5. 5. Neurological & behavioral evidence that STM & LTM exist independently of one another: <ul><li>1. People with hippocampal damage can form STM memories, but cannot form LTM memories. </li></ul><ul><li>2. Head trauma victims have difficulty remembering events just prior to the trauma, but not for memories much earlier than the event. </li></ul><ul><li>3. Retrieval of information from STM is easier than for LTM. </li></ul>
  6. 6. II. Explicit Vs. Implicit memory <ul><li>Explicit memory -- memory for facts or specific events; may be directly tested for by asking the subject questions. </li></ul><ul><li>“ Who is the president of the United States?” </li></ul><ul><li>Implicit memory -- memory that does not require specific events or facts, is largely out of awareness & cannot be directly assessed. </li></ul><ul><li>(riding a bike, shifting gears in car) </li></ul>
  7. 7. III. Declarative Vs. Procedural Memory <ul><li>Declarative memory -- memory that a person can state in words, is based on facts & events. </li></ul><ul><li>---synonymous to explicit memory </li></ul><ul><li>Procedural memory --consists of motor skills. </li></ul><ul><li>---similar to implicit memory (not all implicit memory is motor) </li></ul>
  8. 8. IV. Brain Damage: Explicit Memory impairments! <ul><li>Comes from the case study of H.M (27 yrs) who had severe epileptic seizures that were damaging his brain. </li></ul><ul><li>He elected to have surgeons perform a   </li></ul><ul><li>bilateral medial temporal lobectomy to remove source of seizures. </li></ul><ul><li>Portions of the temporal lobe, hippocampus, & and amygdala were removed. </li></ul>
  9. 9. H.M.—Post Operative <ul><li>H.M.’s personality & intellect were intact. </li></ul><ul><li>His IQ went up a few points & seizures were dramatically reduced. </li></ul><ul><li>However, he had massive memory deficits that radically changed his life. </li></ul>
  10. 10. Memory deficits in H.M. <ul><li>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. </li></ul><ul><li>  </li></ul><ul><li>2. H.M.’s memory for remote events (such as events of his childhood) was intact. </li></ul><ul><li>3. H.M. had profound anterograde amnesia or memory loss for events that occurred following surgery. </li></ul><ul><li>  --He can’t form any new Long Term memories!!!! </li></ul>
  11. 11. Formal Assessment of H.M.’s Anterograde Amnesia: <ul><li>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. </li></ul><ul><li>-After 25 trials of this task, H.M. still could not successfully repeat more than 7 digits (beyond STM span). </li></ul><ul><li>-Most normal Ss can learn up to 18 digits!!! </li></ul>
  12. 12. 2. Verbal and Nonverbal Matching to sample tests : <ul><li>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. </li></ul><ul><li>With verbal stimuli, H.M. did very well & could match the items! In contrast, H.M. performed very poorly with non-verbal stimuli. </li></ul><ul><li>Why???? </li></ul><ul><li>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. </li></ul>
  13. 13. 3. Mirror Drawing Test : <ul><li>H.M. was to draw a line within the boundaries </li></ul><ul><li>of a star-shaped target by watching his hand in a </li></ul><ul><li>mirror (10 trials on 3 consecutive days). </li></ul><ul><li>-Errors (marks out of boundary) were calculated to determine learning. </li></ul><ul><li>  </li></ul><ul><li>-H.M. did well, showing that his implicit motor skill learning ability was intact. However, he had no memory for doing the task . </li></ul><ul><li>  </li></ul>
  14. 14. 4. Rotary-Pursuit Test : <ul><li>H.M. held a stylus in contact with a target rotating on a revolving turntable (record player). </li></ul><ul><li>He did well & improved his performance significantly over 9 daily sessions, despite not recalling doing the task . </li></ul><ul><li>Again, motor skill learning had been spared or preserved. </li></ul><ul><li>But, explicit knowledge of having done the task was not. </li></ul>
  15. 15. The influence of H.M.’s case on search for Neural basis of memory: <ul><li>1. Was the first case to strongly implicate the medial temporal lobes in memory (hippocampus). </li></ul><ul><li>2. H.M.’s case challenged the view that memorial functions are diffusely & equivalently distributed through the brain. </li></ul><ul><li>  </li></ul><ul><li>3. The case provided support for the view of two distinct modes of storage for STM & LTM. </li></ul><ul><li>4. The medial temporal lobes play an important role in memory consolidation. </li></ul>
  16. 16. V. Korsakoffs Syndrome: <ul><li>A disease that develops in individuals who chronically consume alcohol. </li></ul><ul><li>- caused by a thiamine (vitamin B 1) deficiency that occurs almost exclusively in severe alcoholics. </li></ul><ul><li>  </li></ul><ul><li>-memory loss—severe retrograde & anterograde amnesia. </li></ul><ul><li>neurological damage is diffuse, striking damage in dorsal medial nucleus of thalamus, frontal cortex. </li></ul> 
  17. 17. VI. The case of N.A. (1960) <ul><li>N.A. was accidentally stabbed through the right nostril with a fencing foil, that penetrated his skull & went upwards in the forebrain. </li></ul><ul><li>  </li></ul><ul><li>Since the injury he had been unable to retain any new permanent memories & has had great difficulty finding employment. </li></ul><ul><li>CAT scans reveal a small lesion in the left dorsomedial nucleus of the thalamus. </li></ul>
  18. 18. VII. Alzheimer’s Disease: <ul><li>Is a progressive degenerative disease that ultimately results in death , marked by severe retrograde & anterograde amnesia. </li></ul><ul><li>Early onset : late 40’s early 50’s prior to 60’s, is more severe that late onset! </li></ul><ul><li>- Late onset : after 65, we have 50% chance of developing this by age 85. </li></ul>
  19. 19. Alzheimer’s Disease: Symptoms <ul><li>starts with minor forgetfulness (where’s checkbook, etc.) </li></ul><ul><li>Steadily progresses to serious memory loss </li></ul><ul><li>Depression </li></ul><ul><li>Restlessness </li></ul><ul><li>Hallucinations & delusions (seeing dead relatives) </li></ul><ul><li>Anterograde & retrograde amnesia </li></ul>
  20. 20. Alzheimer’s Disease: Genetic basis??? <ul><li>-does seem to run in families, especially in families with early onset. </li></ul><ul><li>-Best evidence--nearly all Down’s Syndrome patients will eventually develop the disease if they survive to middle age. </li></ul><ul><li>-It may depend on at least 2 or 3 different genes </li></ul><ul><li>  </li></ul>
  21. 21. Alzheimer’s Disease: Neurological damage <ul><li>1. There is widespread atrophy of the cortex with plaques & tangles in the hippocampus. </li></ul><ul><li>2. Entorhinal cortex is also destroyed, acetylcholine neurons are diseased. </li></ul><ul><li>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. </li></ul>
  22. 22. Role of hippocampus in memory <ul><li>1. Hippocampus --It is known that the hippocampus is critical in the consolidation of LTM. </li></ul><ul><li>It is thought that infants & young toddlers have early memory problems due to an immature hippocampus. </li></ul><ul><li>Older people with difficulty in explicit memory may show dying or diseased neurons in the hippocampus. </li></ul>
  23. 23. Evidence for hippocampus in memory: <ul><li>1. Case study of H.M. </li></ul><ul><li>2. Alzheimer’s patients (often severe hippocampal damage preceeds most other damage.) </li></ul><ul><li>3. Animal models of hippocampal damage—rats with hippocampal lesions can’t perform 8-arm radial maze task. </li></ul>
  24. 24. What is 8-arm radial maze task? <ul><li>A rat is placed in the center of 8 arms of a maze in which food is placed in the end of the arms. </li></ul><ul><li>Rats have to learn which arms have a unique cue (e.g., rough surface) that signals they have food. </li></ul><ul><li>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. </li></ul><ul><li>In other words, they can’t remember they were there before. </li></ul>
  25. 26. Role of the frontal cortex in memory <ul><li>The prefrontal cortex plays a large role in memory. </li></ul><ul><li>Evidence for this comes from N.A., Korsakoff’s patients, & animal models. </li></ul><ul><li>Prefrontal cortex deteriorates in older age. Aged monkeys perform more poorly on many of the same tasks as do monkeys with prefrontal cortex damage. </li></ul>