Final Exam: Chapter 24 Memory Systems, Chapter 25 Molecular Mechanisms of Learning and Memory Flashcards
learning
- acquisition of new knowledge or skills
- molecular problem involving change in synaptic strength
molecular vs systems problems
- molecular problem: what are molecular mechanisms whereby that storage occurs at each site?
- systems problem: where in the brain are various memories stored?
memory
retention of learned information
declarative memory
memory of facts
temporal lobe; diencephalon
conscious effort
nondeclarative memory
implicit direct experience -procedural memory -classical conditioning -----skeletal musculature (cerebellum) -----emotional responses (amygdala)
non associative learning
-change in behavioral response that occurs over time in response to single type of stimulus (either habituation or sensitization)
habituation
learning to ignore a stimulus that lacks meaning
sensitization
intensifies your response to all stimuli, even those that previously evoked little or no reaction
associative learning
- behavior altered by formation of associations between events
- –classical conditioning
- –instrumental conditioning
classical conditioning
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
instrumental conditioning
individual learns to associate a response (motor act) with meaningful stimulus (typically reward such as food)
why do we study using invertebrate models?
(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)
ex habituation in aplysia
repeated stimulus–>response weakens
- Ca2+ channels open less often with repetition (worn out)
- less opening –> reduced inward Ca2+ –> lower presynaptic Ca2+ –> less NT
- less withdrawal of gill muscle
- muscle habituation
memory storage
sensory information
- ->working memory OR
- –>short term memory
- ——–>with time and consolidation, long term memory
Hebb’s rule 1
-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
cell assembly
- internal representation of object=all cortical cells activated by stimulus
- group of these simultaneously active neurons
- cells are reciprocally interconnected
Hebb’s rule 2
- 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
Morris water maze
- 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
Memory consolidation
- 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
ex sensitization aplysia
-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
long-term potentiation
-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
mechanisms behind LTP
-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
ex classical conditioning aplysia
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)
Synaptic structural changes
-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
Long term depression (LTD)
- Synaptic transmission occuring at same time as strong depolarization of post synaptic neuron causes LTP
- 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
