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Memory and Consolidation

Memory and Consolidation

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Memory and Consolidation

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  1. Memory and Consolidation Prof.dr. Jaap Murre University of Amsterdam University of Maastricht

  2. Overview • Brief review of neuroanatomy of memory • Outline of the TraceLink model • Some simulation results of neural network model, focussing on retrograde amnesia • Memory Chain Model • Forgetting • Amnesia

  3. The Amnesia Paradox • Recent items are remembered best • But they are the first to be lost with (retrograde) amnesia

  4. The Daily News Memory Test at 1810 Dutch respondents

  5. Ribot’s Law: With memory loss, recent memories suffer more Théodule Ribot (1886)

  6. Normal forgetting Ribot Gradient anterograde amnesia retrograde amnesia x present past lesion

  7. Example: Patient data Kopelman (1989) News events test

  8. Neuroanatomy of amnesia • Hippocampus • Adjacent areas such as entorhinal cortex and parahippocampal cortex • Basal forebrain nuclei • Diencephalon

  9. The position of the hippocampus in the brain

  10. Hippocampal connections

  11. Hippocampus has an excellent overview of the entire cortex

  12. The TraceLink Model A model of memory consolidation and amnesia

  13. Trace-Link model: structure

  14. System 1: Trace system • Function: Substrate for bulk storage of memories, ‘association machine’ • Corresponds roughly to neocortex

  15. System 2: Link system • Function: Initial ‘scaffold’ for episodes • Corresponds roughly to hippocampus and certain temporal and perhaps frontal areas

  16. System 3: Modulatory system • Function: Control of plasticity • Involves at least parts of the hippocampus, amygdala, fornix, and certain nuclei in the basal forebrain and in the brain stem

  17. Stages in episodic learning

  18. Dreaming and consolidation of memory “We dream in order to forget” • Theory by Francis Crick and Graeme Mitchison (1983) • Main problem: Overloading of memory • Solution: Reverse learning leads to removal of ‘obsessions’

  19. Dreaming and memory consolidation • When should this reverse learning take place? • During REM sleep • Normal input is deactivated • Semi-random activations from the brain stem • REM sleep may have lively hallucinations

  20. Consolidation may also strengthen memory • This may occur during deep sleep (as opposed to REM sleep) • Both hypothetical processes may work together to achieve an increase in the clarity of representations in the cortex

  21. Difficult visual discrimination problem Several hours of practice One group goes home Other group stays in the lab and skips a night of sleep Experiment by Robert Stickgold

  22. Improvement without further training due to sleep Normal sleep Skipped first night sleep

  23. Relevant animal data by Matt Wilson and Bruce McNaughton (1994) • 120 neurons in rat hippocampus • PRE: Slow-wave sleep before being in the experimental environment (cage) • RUN: During experimental environment • POST: Slow-wave sleep after having been in the experimental environment

  24. Wilson en McNaughton Data • PRE: Slow-wave sleep before being in the experimental environment (cage) • RUN: During experimental environment • POST: Slow-wave sleep after having been in the experimental environment

  25. Some important characteristics of amnesia • Anterograde amnesia (AA) • Implicit memory preserved • Retrograde amnesia (RA) • Ribot gradients • Pattern of correlations between AA and RA • No perfect correlation between AA and RA

  26. Normal forgetting Amnesia patient anterograde amnesia retrograde amnesia x present lesion past

  27. Example of patient data Kopelman (1989) News events test

  28. Retrograde amnesia • Primary cause: loss of links • Ribot gradients • Shrinkage

  29. Anterograde amnesia • Primary cause: loss of modulatory system • Secondary cause: loss of links • Preserved implicit memory

  30. Semantic dementia • The term was adopted recently to describe a new form of dementia, notably by Julie Snowden et al. (1989, 1994) and by John Hodges et al. (1992, 1994) • Semantic dementia is almost a mirror-image of amnesia

  31. Neuropsychology of semantic dementia • Progressive loss of semantic knowledge • Word-finding problems • Comprehension difficulties • No problems with new learning • Lesions mainly located in the infero-lateral temporal cortex but (early in the disease) with sparing of the hippocampus

  32. No consolidation in semantic dementia Severe loss of trace connections Stage-2 learning proceeds as normal Stage 3 learning strongly impaired Non-rehearsed memories will be lost

  33. Semantic dementia in TraceLink • Primary cause: loss of trace-trace connections • Stage-3 (and 4) memories cannot be formed: no consolidation • The preservation of new memories will be dependent on constant rehearsal

  34. Connectionist implementationof the TraceLink model With Martijn Meeter

  35. Some details of the model • 42 link nodes, 200 trace nodes • for each pattern • 7 nodes are active in the link system • 10 nodes in the trace system • Trace system has lower learning rate that the link system

  36. How the simulations work: One simulated ‘day’ • A new pattern is activated • The pattern is learned • Because of low learning rate, the pattern is not well encoded at first in the trace system • A period of ‘simulated dreaming’ follows • Nodes are activated randomly by the model • This random activity causes recall of a pattern • A recalled pattern is than learned extra

  37. (Patient data) Kopelman (1989) News events test

  38. A simulation with TraceLink

  39. Frequency of consolidation of patterns over time

  40. Strongly and weakly encoded patterns • Mixture of weak, middle and strong patterns • Strong patterns had a higher learning parameter (cf. longer learning time)

  41. Transient Global Amnesia (TGA) • (Witnessed onset) of severe anterograde and retrograde amnesia • Resolves within 24 hours • Retrograde amnesia may have Ribot gradients • Hippocampal area is most probably implicated

  42. Transient Global Amnesia (TGA)

  43. Other simulations • Focal retrograde amnesia • Implicit memory • More subtle lesions (e.g., only within-link connections, cf. CA1 lesions) • Semantic dementia • Schizophrenia (memory effects in -) with an extended model (added parahippocampal layer)

  44. Alternative Explanations • ‘Memory Bump’ appears as reverse gradient • Nadel and Moscovitz (1997): Trace Replication Theory (will be discussed next time by the students)

  45. Sir Francis Galton (1879) • Inspected a cue word, e.g., coffee until an event came to mind • Later, he dated the events

  46. Lifetime distributions • The Galton-Crovitz method aims for a quasi-random sample of autobiographical memories • Stratified through the use of keywords • Technically speaking: The method measures a probabilitydensity function of memory age

  47. Rubin, Wetzler & Nebes (1986) • Found a reminiscence bump between 10 and 30 years, when older than 40 years.

  48. Herinneringsbobbel (Rubin, et al., 1986)

  49. Large-scale replication using the internet • Website: Steve Janssen Antonio Chessa