Learning and Memory

1. Learning and Memory Dr. Kline FSU-PC

2. What is memory? • What do you think???

3. 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?)

4. What is the process by which STM is transferred to LTM? • What do you think??? • Consolidation

5. 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.

6. 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)

7. 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)

8. 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.

9. 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.

10. 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!!!!

11. 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!!!

12. 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.

13. 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 3consecutive 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.

14. 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.

15. 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.

16. 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.

17. 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.

18. 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.

19. 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

20. 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

21. 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.

22. 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.

23. 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.

24. 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.

26. 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.