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Pinel basics ch09

May 11, 2015



  • 1.Chapter 9 Learning, Memory, and Amnesia How Your Brain Stores Information
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2. The Brain Changes its Functioning in Response to Experience

  • Learning how experience changes the brain
  • Memory how changes are stored and subsequently reactivated
  • What brain structures are involved in processes of learning and memory?

3. Effects of Bilateral Medial Temporal Lobectomy

  • H.M. an epileptic who had his temporal lobes removed in 1953
  • His seizures were dramatically reduced but so was his memory
  • Mild retrograde amnesia and severe anterograde amnesia

4. Amnesia

  • Retrograde (backward-acting) unable to remember the past
  • Anterograde (forward-acting) unable to form new memories
  • While H.M. is unable to form most types of new long-term memories, his STM is intact

5. Assessing H.M.

  • Digit span H.M. can repeat digits as long as the time between learning and recall is within the limits of short-term storage
  • Mirror-drawing task H.M. exhibits improvement with practice. He is able to show skill memory demonstrating that he can learn some things (also rotary-pursuit and a drawing task) although he is not aware of it

6. Assessing H.M.

  • H.M. readily learns responses through Pavlovian (classical) conditioning
  • H.M. can learn some things, but has no memory of having learned them

7. Scientific Contributions of H.M.s Case

  • Medial temporal lobes are involved in memory
  • Short-term memory (STM) and long-term memory (LTM) are distinctly separate
  • H.M. is unable to move memories from STM to LTM, a problem with memory consolidation

8. Scientific Contributions of H.M.s Case

  • Memory may exist but not be recalled as when H.M. exhibits a skill he does not know he has learned
  • H.M. forms new implicit memories, but not new explicit memories

9. Explicit Vs Implicit Memories

  • Explicit memories conscious memories
  • Implicit memories unconscious memories, as when H.M. shows the benefits of prior experience
  • Repetition priming tests used to assess implicit memory performance in identifying word fragments is improved when the words have been seen before

10. Medial Temporal Lobe Amnesia

  • Not all with this form of amnesia are unable form new explicit long-term memories as was the case with H.M.
  • 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)

11. 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

12. Korsakoffs Syndrome

  • Most commonly seen in who?
  • Alcoholics
  • Also seen in individuals with a thiamine-deficient diet
  • Alcohol causes a disruption in the bodys ability to use thiamine

13. Korsakoffs Syndrome

  • Characterized by amnesia, confusion, personality changes, and physical problems
  • Typically damage in the medial diencephalon medial thalamus + medial hypothalamus

14. Korsakoffs Syndrome

  • Amnesia comparable to medial temporal lobe amnesia in the early stages
    • Anterograde amnesia for episodic memories
  • Differs in later stages
    • Severe retrograde amnesia develops
  • Differs in that it is progressive, complicating its study

15. What damage causes the amnesia seen in Korsakoffs?

  • Hypothalamic mammillary bodies?
    • No Korsakoffs amnesia is seen in cases without such damage
  • Thalamic mediodorsal nuclei?
    • Possibly damage is seen here when there is no mammillary damage
  • Cause is not likely to be damage to a single diencephalic structure

16. Alzheimers Disease (AD)

  • Begins with slight loss of memory and progresses to dementia
  • General deficits in predementia AD
    • Major anterograde and retrograde amnesia in explicit memory tests
    • Deficits in STM and some types of implicit memory verbal and perceptual
  • Implicit sensorimotor memory is intact

17. What damage causes the amnesia seen in AD?

  • Decreased acetylcholine
    • Due to basal forebrain degeneration
    • Basal forebrain strokes can cause amnesia and attention deficits which may be mistaken for memory deficits
  • Medial temporal lobe and prefrontal cortex also involved
  • Damage is diffuse resulting amnesia is likely a consequence of acetylcholine depletion and brain damage

18. Posttraumatic Amnesia

  • Concussions may cause retrograde amnesia for the period before the blow and some anterograde amnesia after
  • The same is seen with comas, with the severity of the amnesia correlated with the duration of the coma
  • Period of anterograde amnesia suggests a temporary failure of memory consolidation

19. Gradients of RetrogradeAmnesia and Memory Consolidation

  • Concussions disrupt consolidation (storage) of recent memories
  • Hebb memories are stored in the short term by neural activity
  • Interference with this activity prevents memory consolidation
    • Blows to the head (i.e., concussion)
    • ECS (electroconvulsive shock)

20. The Hippocampus and Consolidation

  • What role does the hippocampus play in consolidation?
  • Some have proposed that memory storage structures store memories for as long as they exist and eventually an engram forms
  • Engram a change in the brain that stores a memory

21. Object-Recognition Memory

  • Early animal models of amnesia involved implicit memory and assumed the hippocampus was key
  • 1970s monkeys with bilateral medial temporal lobectomies show 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)

22. Testing object-recognition memory 23. Delayed Nonmatching-to-Sample Test for Rats

  • Aspiration used to lesion the hippocampus in monkeys resulting in additional cortical damage
  • Extraneous damage is limited in rats due to lesion methods used
  • Bilateral damage to rat hippocampus, amygdala, and rhinal cortex produces the same deficits seen in monkeys with hippocampal lesions

24. Object-Recognition Deficits andMedial Temporal Lobectomy

  • Neuroanatomical basis of resulting deficits?
  • Bilateral removal of the rhinal cortex > object-recognition deficits
  • Bilateral removal of the hippocampus > no or moderate effects on object recognition
  • Bilateral removal of the amygdala?
    • No effect on object-recognition.

25. A Paradox

  • Removing the hippocampus has a moderate effect on object recognition while ischemia-induced lesions to a small part of it leads to severe deficits
  • How can this be?

26. A Hypothesis

  • Ischemia-induced hyperactivity of CA1 pyramidal cells damages neurons outside of the hippocampus
  • Extrahippocampal damage not readily detectable
  • Extrahippocampal damage is largely responsible for ischemia-induced object recognition deficits.
  • Evidence?

27. A Hypothesis

  • Ischemia-induced hyperactivity leads to extrahippocampal damage that explains ischemia-induced object recognition deficits
    • Bilateral hippocampectomy prevents ischemia-induced deficits
    • Supported by functional brain-imaging studies

28. The Hippocampus

  • Rhinal cortex plays an important role in object recognition
  • Hippocampus plays a key role in memory for spatial location
    • Hippocampal lesions producesdeficits on Morris water and radial arm mazes
    • Many hippocampal cells are place cells responding when a subject is in a particular place

29. 30. Comparative Studies of the Hippocampus

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