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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

memory

A

retention of learned information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

declarative memory

A

memory of facts
temporal lobe; diencephalon
conscious effort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

nondeclarative memory

A
implicit
direct experience
-procedural memory
-classical conditioning
-----skeletal musculature (cerebellum)
-----emotional responses (amygdala)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

habituation

A

learning to ignore a stimulus that lacks meaning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

sensitization

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

associative learning

A
  • behavior altered by formation of associations between events
  • –classical conditioning
  • –instrumental conditioning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

instrumental conditioning

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

memory storage

A

sensory information

  • ->working memory OR
  • –>short term memory
  • ——–>with time and consolidation, long term memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Long term depression (LTD)

A
  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