12: synaptic plasticity

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what happens in the correlation test of the inferior olive (IO)

neurons in the IO respond when the US (air puff) is delivered to a naive animal

what happens in the necessity test of the IO

when IO is lesioned, the CR functions as if US is absent

prevent acquisition of CR and extinction

what happens in the sufficiency test of the IO

electrical stimulation of the IO can substitute for the US (CR will still develop with nothing happening)

what are the 2 glutamate receptors in post-synaptic interpositus neurons

AMPA & NMDA

what kind of ion is Mg2+ and what role does it play in interpositus neurons

divalent cation, blocks NMDA receptors

what happens during the pretraining (baseline) neural response to only the CS

pontine neurons fire & release glutamate onto interpositus neurons

glutamate binds to AMPA & NMDA receptors but only AMPA receptors pass current since NMDA is blocked by Mg2+

sodium through AMPA generates EPSP, but too small to trigger AP because there are few AMPA receptors in mossy fiber synapse

what happens during the pretraining (baseline) neural response to only the US

IO neurons fire & release glutamate onto interpositus neurons which generates EPSP

EPSP triggers AP in interpositus because lots of AMPAR in climbing fiber synapse

depolarization causes Mg2+ off NMDAR at mossy fiber

what happens during the training (CS-US paring) phase

CS causes pontine neurons to fire & release glutamate on weak interpositus synapses while US causes IO to fire & release glutamate on strong synapses

since Mg2+ is no longer on NMDAR, it allows Ca2+ to enter interpositus

what is the process of long-term potentiation (LTP)

Ca2+ entry through NMDARs activates calmodulin (CAM) which activates CAM kinase II (CAMKII)

CAMKII triggers signaling that leads to insertion of more AMPA receptors into postsynaptic membrane of mossy fiber synapse, making synapse stronger

what happens during post-training (testing) neural response to CS

pontine neurons fire & release glutamate onto interpositus

mossy fiber synapse generates large EPSP that triggers AP in postsynaptic (eyeblink) and opens NMDA receptors

hebb’s rule (1949)

when 2 cells are active at same time, the synapse between them becomes stronger & stays stronger for a long time after

what is coincidence detection

part of hebb’s rule that requires a biological mechanism to signal when pre and postsynaptic cell are activated at same time

how does NMDA play into the conditioning process

NMDARs are necessary for acquisition but not expression of eyeblink CR when NMDAR antagonist (AP5) is infused into interpositus

where is the amygdala located and what does it control

temporal lobe, controls fear, anxiety, and emotions

what are the 2 parts of the amygdala and what do they consist of

striatal amygdala: inhibitory projection neurons, central (Ce) & medial (M) nuclei

cortical amygdala complex: excitatory projection neurons, lateral (LA), basal (B), accessory basal (AB) nuclei

what parts of the amygdala are necessary for learning auditory fear conditioning

lateral and central nuclei

what is the process of synaptic plasticity during auditory fear conditioning

nociceptive inputs by footshock are sent to LA nucleus which excites neurons in Ce nucleus

Ce sends inhibitory projections to ventral periaqueductal gray (vPAG) which disinhibits neurons to drive freezing

what is the difference in the process of conditioning and fear conditioning

presynaptic comes from thalamus or cortex (CS) and postsynaptic is in LA nucleus

what happens when LA neurons are optogenetically stimulated instead of US

rats would learn to freeze from the light rather than an actual shock but it was only about 25% of the time

what are the stages of memory in order and how long are they

iconic: briefest, few seconds

short term: aka working memory, one minute

intermediate-term: hours/days

long-term: months, years, lifetime

how are long-term memories made

CAM triggers adenyl cyclase to convert ATP to cAMP which activates protein kinase (PKA)

PKA phosphorylates mitogen-activated protein kinase (MAPK)

MAPK goes to soma and enters nucleus of LA, activating CREB

CREB activates gene transcription, producing mRNA that transcribes into new proteins

new proteins are materials for new dendritic spines on the LA neuron

what is anisomycin

a drug that blocks protein synthesis

how does protein synthesis affect fear conditioning

when anisomycin is infused in amygdala, long term memory is impaired for CS-US association (no freezing after a certain amount of time)