Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
33 Cards in this Set
- Front
- Back
|
Hebb's hypothesis of memory |
cells that fire together, wire together |
|
|
where does memory occur? |
at the level of the synapse |
|
|
what is procedural learning? |
results in an action / movement (cerebellum involvement) |
|
|
what are the two types of non-associative learning? |
1. habituation - learning to ignore stimulus without meaning 2. sensitization - learning to intensify response to stimuli (blackout in the street) |
|
|
what is pavlovian conditioning? |
pavlovian conditioning = classical conditioning - makes associations with two stimuli - unconditioned stimulus must come directly before or at the same time as the conditioned stimulus |
|
|
what is instrumental conditioning? |
- meaningful stimulus (catheter lever bar) - has a motivation component to it |
|
|
In aplysia, what type of non-associative learning occurs? |
- habituation occurs after continual stimulation, which occurs at the synapse through synaptic modification |
|
|
what kinase does cAMP work with? |
protein kinase A (PKA) |
|
|
how does 5-HT work to increase neurotransmitter release? |
5-HT activates PKA, PKA inhibits potassium channels; calcium builds in the cell since cell has prolonged depolarization - neurotransmitter release increases |
|
|
when does plasticity occur pre synaptically? |
presynaptic modification = between sensory and motor |
|
|
how is aplysia used for classical conditioning? |
- tactile stimulus is paired with a shock - causes changes and presynaptic learning - shock induces a 5-HT response - 5-HT activates PKA, which increases cAMP, which decreases open potassium channels, which prolongs the depolarization, leading to an increase of [Ca], leading to an increase in neurotransmitter release |
|
|
what are the two types of plasticity and what type of stimulation are they associated with? |
- LTP - associated with high freq stimulation (HFS); tetanus shots cause short-term plasticity; LTP = increased response for more than one hour - LTD - associated with low frequency stimulation (LFS) |
|
|
What are some induction protocols for synaptic plasticity? |
1. HFS (for LTP) 2. LFS (for LTD) 3. pairing protocol (for whole cell recording); conduct postsynaptic depolarization ICW LFS 4. primed burst stimulation (physiological plasticity) 5. theta burst stimulation (physiological plasticity) 6. spike timing dependent plasticity (STDP) |
|
|
what is an example of a short-term plasticity mediator? |
- endocanabinoid-mediated short-term synaptic plasticity |
|
|
what are some properties of purkinje cells in the cerebellum? |
- dendrites only go into the molecular layer - cell axons synapse deep within the cerebellar nuclei - GABA = neurotransmitter |
|
|
Where does the climbing fiber come from and where does it go and what does it do? |
- originates in the superior olive - wraps itself around the purkinje cell - gives error input - one climbing fiber can depolarize the purkinje cell |
|
|
Where does the granule cell come from and where does it go and what does it do? |
- originates from the midbrain - goes to the parallel fiber |
|
|
where does learning occur in the cerebellum? |
- at the synapse of the parallel fiber and purkinje cell |
|
|
how can you study learning in the cerebellum? |
- stimulate the climbing fiber and parallel fiber - record from purkinje cell - induction protocol: pair the stimulating of climbing and parallel fibers to create coincidence effector - creates LTD at the synapse of purkinje and parallel, resulting in learning (GABA = neurotransmitter) |
|
|
what molecular changes occur in the purkinje cell during learning? |
- uses mGluR (a GPCR) - metabotropic receptor - mGluR activates DAG, which activates PKC (protein kinase C) |
|
|
what is all plasticity dependent on? |
calcium |
|
|
what is the flow of projections in the hippocampus? |
entorhinal cortex to the dentrate gyrus to the CA3 to the CA1 |
|
|
how can you study LTP in the hippocampus? |
- LTP in the CA1 is input-specific - tetanize one pathway, but not the other and then compare the output/recording from both - postsynaptic LTP in CA1: NMDAR = coincident detector: you need both glutamate and depolarization (to remove Mg block) for NMDAR; record AMPA current |
|
|
what happens presynaptically during LTP? |
- there is a rush of calcium in the presynaptic terminal to release more neurotransmitter |
|
|
what happens postsynaptically during LTP? |
- kinases up-regulate receptors in the membrane through phosphorylation - AMPA receptors |
|
|
what is the BCM theory? |
- at low NMDA activation, LTD occurs - as NMDA activation increases, it changes from LTD to LTP because the synaptic strength increases (looks like a sine wave on graph) |
|
|
when there is weak depolarization, what type of plasticity occurs? |
- LTD occurs due to Ca removing phosphorylation (thereby removing AMPARs aka down-regulating) |
|
|
What induces LTP and LTD in spike-timing dependent plasticity? |
- LTP = pre-post AP pairing - LTD = post-pre AP pairing |
|
|
What does LTP do at an excitatory synapse vs an inhibitory synapse? |
- excitatory synapse: LTP increases glutamate thereby increasing excitability - inhibitory synapse: LTP increases GABA thereby increasing inhibition |
|
|
homeostatic plasticity principle |
- homeostatic plasticity is always trying to return to the basal state |
|
|
how is plasticity maintained (for long-term modification)? |
1. CAMKII and LTP: CAMKII removes the requirement of Ca for phosphorylation because CAMKII auto-phosphorylates itself 2. protein synthesis is required for maintenance of plasticity |
|
|
what is the concept of coincidence timing? |
- if you add channels, resistance decreases (becomes more leaky), so you need more current to reach threshold for AP |
|
|
how does temperature effect the incident detection window? |
- increasing temperature decreases the incident detection windown |
