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what part of Henry Molaisons (HM) brain was removed during surgery?
- majority of the temporal lobes;
- amygdala
- hippocampus
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what effects did HM experience
- anterograde amnesia -> moving forward
- retrograde amnesia
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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)
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retrograde amnesia in HM
- few memories from a decade before surgery (highschool graduation, WW2)
- memories before that time were intact
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anterograde vs. retrograde
an impairment in forming new memories vs. the inability to remember events prior to impairment
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consolidation
process in which the brain forms a more or less permanent physical representation of a memory
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retrieval
process of accessing stored memories
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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
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role of prefrontal cortex
directs the search strategy for retrieval only
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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)
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declarative memory
- learning that results in memories of facts, people, and events that a person can verbalize or declare
- WHAT
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non-declarative memory
- memories for behaviors
- results from procedural/skills learning, emotional learning, and stimulus response conditioning
- HOW
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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)
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working memory
- provides a temporary "register" for the info while it is being used (phone numbers, chess move, conversations)
- chunking (ROYGBV, NESW, ACC football)
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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
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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
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long term potentiation (LTP)
- increase in synaptic strength when both neurons activated
- hippocampus and other "learning" areas
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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"
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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
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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
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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%
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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
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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
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neurogenesis
- additional changes during learningincreases in the hippocampus (10-20% increase in life)
- ->new neurons more likely to participate in learning (London cabbies)
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consolidation enzymes
- CaMKII
- protein kinase Mzeta
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consolidation enzyme: CaMKII
- critical for establishment of LTP
- ->doesn't reverse LTP once is it established when inhibited
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consolidation enzyme: Protein Kinase Mzeta
- maintains long term memory
- ->inhibition causes amnesia for already established conditioned responses
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changing memories: extinction
- changing memories
- new learning
- requires NMDA (like LTP)
- ->blocking receptors eliminates extinction
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changing memories: forgetting
- active, adaptive biological process
- protein phophhate 1 (PP1) and protein RAC produce memory loss after learning
- forgetting prevents saturation of synapses
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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
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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
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alzheimers projection
- number of people with this disease will increase by 350% by 2050 (14.3 million people)
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