Final Exam: Chapter 24 Memory Systems, Chapter 25 Molecular Mechanisms of Learning and Memory Flashcards

1
Q

learning

A
  • acquisition of new knowledge or skills

- molecular problem involving change in synaptic strength

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2
Q

molecular vs systems problems

A
  • molecular problem: what are molecular mechanisms whereby that storage occurs at each site?
  • systems problem: where in the brain are various memories stored?
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3
Q

memory

A

retention of learned information

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4
Q

declarative memory

A

memory of facts
temporal lobe; diencephalon
conscious effort

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5
Q

nondeclarative memory

A
implicit
direct experience
-procedural memory
-classical conditioning
-----skeletal musculature (cerebellum)
-----emotional responses (amygdala)
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6
Q

non associative learning

A

-change in behavioral response that occurs over time in response to single type of stimulus (either habituation or sensitization)

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7
Q

habituation

A

learning to ignore a stimulus that lacks meaning

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8
Q

sensitization

A

intensifies your response to all stimuli, even those that previously evoked little or no reaction

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9
Q

associative learning

A
  • behavior altered by formation of associations between events
  • –classical conditioning
  • –instrumental conditioning
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10
Q

classical conditioning

A

associating a stimulus that evokes measurable response with second stimulus that normally does not evoke this response
-the learned response to the conditioned stimulus=conditioned response

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11
Q

instrumental conditioning

A

individual learns to associate a response (motor act) with meaningful stimulus (typically reward such as food)

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12
Q

why do we study using invertebrate models?

A

(aplysia californica or drosophila melanogaster)

  • in invertebrates, changes are presynaptic; vertebrates, changes=post synaptic
  • small nervous system
  • large neurons
  • identifiable neurons (classified by size, location)
  • identifiable circuits
  • ability to learn
  • simply genetics (small genomes, rapid life cycles)
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13
Q

ex habituation in aplysia

A

repeated stimulus–>response weakens

  1. Ca2+ channels open less often with repetition (worn out)
  2. less opening –> reduced inward Ca2+ –> lower presynaptic Ca2+ –> less NT
  3. less withdrawal of gill muscle
  4. muscle habituation
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14
Q

memory storage

A

sensory information

  • ->working memory OR
  • –>short term memory
  • ——–>with time and consolidation, long term memory
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15
Q

Hebb’s rule 1

A

-learning=synaptic strengthening
-pre and post synaptic coactivation
-when axon of cell A excites cell B and repeatedly and persistently takes part in firing it, some growth process/metabolic process takes place in one or both of the cells so that A’s efficiency, as one of the cells firing B, is increased
-or, when presynaptic axon is active and, at the same time, the post synaptic neuron is STRONGLY activated by other inputs, synapse=strengthened
…If activation of cell assembly persists for long enough, consolidation occurs by growth process
-neurons that fire together are wired together
-cell assembly held in working memory unless it undergoes this process

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16
Q

cell assembly

A
  • internal representation of object=all cortical cells activated by stimulus
  • group of these simultaneously active neurons
  • cells are reciprocally interconnected
17
Q

Hebb’s rule 2

A
  • forgetting=synaptic weakening
  • presynaptic activity does not cause post synaptic activity
  • when pre synaptic axon is active and, at the same time, post synaptic neuron is WEAKLY activated by other inputs, synapse is weakened
  • neurons that fire out of sync lose their link
18
Q

Morris water maze

A
  • hippocampus necessary for spacial memory
  • ->mice with bilateral hippocampal damage never figure out/remember location of platform
  • place field evokes greatest response, place cells
  • block NMDA receptor is blocking spatial memory
19
Q

Memory consolidation

A
  • process by which some experiences (which are being held temporarily by transient modifications of neurons) are selected for permanent storage in long term memory
  • changes short term memory to long term
20
Q

ex sensitization aplysia

A

-strong noxious stimulus–> strong response returns
STEPS
1. apply brief electrical shock to head of aplysia
2. 5-HT released presynaptically by L29 onto the sensory neuron
3. G protein coupled receptor activated
–>activates Adenyl cyclase
—–>production of cAMP from AMP
———>activates protein kinase A (PKA)
4. Protein kinase A attaches PO4 to K+ channels
–>channels close
5. decrease in K+ conductance, prolongs action potential
6. More Ca2+ entry
–>more NT release per AP
—–>gill withdrawal reflex restored

21
Q

long-term potentiation

A

-hippocampus (critical for memory formation)
-high freq electrical stimulation: tetanus
-induces LTP and subsequent test stimulation evokes EPSP much greater
-modification of stimulated synapses so that they are more effective
-Input specificity: only active inputs show synaptic plasticity
*however, tetanus not always required – just need synapses active at the same time post synaptic CA1 neuron depolarized (this is often caused by the tetanus though)
+ COOPERATIVITY: coactive synapses must cooperate enough to produce enough depolarization to cause LTP

22
Q

mechanisms behind LTP

A

-CA1 neurons have NMDA receptors
(review)
-only conduct Ca2+ when
1. glutamate binds and
2. post synaptic membrane depolarized enough to displace MG2+
AMPA: ligand gated; conducts Na
NMDA: ligand and voltage gated; conducts Na and Ca

23
Q

ex classical conditioning aplysia

A

US=strong shock of tail
R=withdrawal of gill
CS=gentle stimulation of siphon
-like during sensitization, 5-HT
-but also Ca2+ acts at same time
——-
-CS + US=greater activation of adenyl cyclase becase CS increases Ca2+
-increase in sensitivity to G protein activation
-learning: Ca2+ and 5-HT coincide, increase cAMP, increase protein kinase activity (PKA)

24
Q

Synaptic structural changes

A

-occur after LTP
-sprouting synapses increases responsive post synaptic surface, increases probability of AP triggering presynaptic glutamate release
PRESYNAPTIC CHANGES
-amount of NT released
-size of presynaptic terminal
-number of axon terminals (sprouting)
POST SYNAPTIC CHANGES
-Phosphorylation of AMPA receptor
-externalization of AMPA and NMDA receptors
-synthesis of new AMPA and NMDA receptors
-increase in size of post synaptic element
-changes in spine shape

25
Long term depression (LTD)
1. Synaptic transmission occuring at same time as strong depolarization of post synaptic neuron causes LTP 2. synaptic transmission at the same time as weak/modest depolarization, LTD * *difference is in NMDA activation - with only weak depolarization, partial blockage of channels by Mg2+, not enough Ca2+ entering - with stronger depolarization, Mg2+ displaced, Ca2+ levels activate protein phosphatases (enzymes that take phosphate groups off proteins) - ->LTP is putting phosphate groups on, LTD is taking them off