learning memory

  1. what part of Henry Molaisons (HM) brain was removed during surgery?
    • majority of the temporal lobes; 
    • amygdala 
    • hippocampus
  2. what effects did HM experience
    • anterograde amnesia -> moving forward 
    • retrograde amnesia
  3. anterograde amnesia in HM
    • formed new memories for the next 55 years
    • within minutes a new memory would disappear 
    • could remember well rehearsed information (house layout)
  4. retrograde amnesia in HM
    • few memories from a decade before surgery (highschool graduation, WW2)
    • memories before that time were intact
  5. anterograde vs. retrograde
    an impairment in forming new memories vs. the inability to remember events prior to impairment
  6. consolidation
    process in which the brain forms a more or less permanent physical representation of a memory
  7. retrieval
    process of accessing stored memories
  8. role of glutamate
    • works in both consolidation and retrieval 
    • blocking the receptors for 7 days following learning prevents the memory from being consolidated 
    • blocking them during testing interferes with retrieval
  9. role of prefrontal cortex
    directs the search strategy for retrieval only 
  10. where are memories stored?
    • temporally in the hippocampal formation
    • overtime memory is moved to cortical areas; stored where information was processed (verbal stored in left frontal lobe)
  11. declarative memory
    • learning that results in memories of facts, people, and events that a person can verbalize or declare
    • WHAT
  12. non-declarative memory
    • memories for behaviors
    • results from procedural/skills learning, emotional learning, and stimulus response conditioning
    • HOW 
  13. two kinds of learning
    • different origins in the brain
    • radial arm rate maze
    • nondeclarative with hipocampal damage (learned)
    • declarative with striatum damage (memories)
    • amygdala has significant role in non-declarative emotional learning (strengthens declarative memories about emotional events)
  14. working memory
    • provides a temporary "register" for the info while it is being used (phone numbers, chess move, conversations)
    • chunking (ROYGBV, NESW, ACC football)
  15. prefrontal cortex in working memory
    • works in tandem with sensory association areas (repeating sounds)
    • acts as working memory central executive
    • ->manages behavioral strategies and decision making
    • ->directs neural traffic in working memory
    • ->coordinates activity involved in perception and response
  16. hebb rule
    • if an axon of a pre-synaptic neuron is active while post-synaptic neuron is firing, synapse will be strengthened 
    • ->how neurons are selected for survival during development 
    • basis for learning
  17. long term potentiation (LTP)
    • increase in synaptic strength when both neurons activated 
    • hippocampus and other "learning" areas
  18. long term depression (LTD)
    • decrease in strength of synapses when pre-synaptic neurons insufficient to activate post-synaptic cells 
    • how brain modifies or clears memories
    • "unlearning"
  19. associative long term potentiation
    • pre-synaptic neurons influence sensitivity of nearby synapses 
    • may underlie classical conditioning 
    • -> auditory stimulus paired with shock=amygdala and fear behavior
  20. LTP/LTD and relationship to theta waves
    • triggered by theta activity (4-7 Hz)
    • ex: rats don't learn mazes during theta suppression
    • ->theta in hippocampus during novelty
    • ->LTP enhanced during theta peak, reversed at toughs
  21. neuro-chemical processes in LTP
    • LTP requires a sequence of events 
    • ->glutamate activates AMPA
    • ->NMDA blocked by Mg ions
    • first pulse partially depolarizes membrane and dislodge Mg ions 
    • further stimulation activates NMDA, depolarizing the membrane 
    • CA2+ influx activates enzyme, CaMKII, strengthening the synapse 
    • ->CaMKII dysregulation linked with alzheimers
    • ->when missing, LTP decreases 50%
  22. neuro-chemical processes in LTP
    • dedrite, much depolarized
    • ->if activation is strong enough to depolarize partially the post-synaptic membrane, the Mg ions are ejected 
    • -NMDA receptor can be activated, allowing sodium and calcium ions to enter
  23. nitric acid
    • released by the post-synaptic neuron when its activated 
    • diffuses across the cleft to the pre-synaptic neuron, where it induces the neuron to release more neurotransmitter
    • causes for:
    • ->an increased number of dendric spins
    • ->enlargement/splitting of existing spines
    • ->transport of additional AMPA receptors into spines
    • makes the synapse more sensitive
  24. neurogenesis
    • additional changes during learning
    • increases in the hippocampus (10-20% increase in life)
    • ->new neurons more likely to participate in learning (London cabbies)
  25. consolidation enzymes
    • CaMKII
    • protein kinase Mzeta
  26. consolidation enzyme: CaMKII 
    • critical for establishment of LTP
    • ->doesn't reverse LTP once is it established when inhibited
  27. consolidation enzyme: Protein Kinase Mzeta
    • maintains long term memory 
    • ->inhibition causes amnesia for already established conditioned responses
  28. changing memories: extinction
    • changing memories
    • new learning 
    • requires NMDA (like LTP)
    • ->blocking receptors eliminates extinction
  29. changing memories: forgetting
    • active, adaptive biological process
    • protein phophhate 1 (PP1) and protein RAC produce memory loss after learning 
    • forgetting prevents saturation of synapses
  30. reconsolidation
    • when a memory is retrieved
    • opportunity to refine memories and correct errors
    • ->modify your emotional experience (therapy for phobias)
    • can result in memory reconstruction and "recall" of false memories 
  31. alzheimers
    • most common cause of dementia
    • progressive brain deterioration and declarative (memory loss)
    • most behaviors suffer 
    • ->language
    • ->visual-spatial functions
    • ->reasoning 
    • effects increase with age 
    • ->10% over 65
    • ->50% over 85
  32. alzheimers projection
    • number of people with this disease will increase by 350% by 2050 (14.3 million people)
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Author
casiemarie
ID
253384
Card Set
learning memory
Description
final exam
Updated