CH.8 Synaptic Plasticity

what is synaptic plasticity?

activity changes in synaptic response and properties

what is potentiation?

strengthening a synapse, works for a longer period, move vesicles from ready to reserve, relies on PKC and kinases

what is augmentation?

works for a shorter time period, triggered by chemical changes and efficiency of Ca2+

what is synaptic depression?

caused by rapid depletion of synaptic vesicles, they are spent faster than recycled

what is facilitation?

leftover Ca2+ from first neurotransmitter release boosts the transmitter power of a second release

what is habituation (includes aplysia model explanation)?

less response to a repeated stimuli, repeated light touch to siphon lessens gill contraction, sensory neurons continue to fire and motor neurons do not get a pre-synaptic potential

what is sensitization?

large response generated from aversive stimuli, electric shock to tail causes siphon to shoot more, reinstates pre-synaptic response

what is short-term plasticity based on?

presynaptic and chemical changes, repeated activation of a chemical synapse

what are the different mechanisms of short-term plasticity?

facilitation, potentiation, depression, augmentation

Aplysia model circuit main premise (sensitization)

the modultatory interneuron amplifies the signal by facilitated synaptic activity with serotonin

Aplysia model circuit main premise (habituation)

when stimulating the siphon, the response travels to an interneuron or motor neuron directly

What is the mechanism for the sensitization circuit (Aplysia model)

serotonin binds to serotonin receptor, G-protein converts GDP to GTP and causes a conformational change, adenylyl cylclase breaks into cAMP, cAMP activates PKA which phosphorylates potassium channel and enhances calcium channel, glutamate is released on the receptor

how does long-term plasticity work?

modifies genes

how does long-term potentiation work?

requires a strong stimulation of NMDA and schaeffer collaterals, Ca2+ binds to NMDA and triggers a PKC or CaMKII to phosphorylate a protein binding to AMPA

how does long-term depression work?

requires a weak signal of NMDA and schaeffer collaterals, Ca2+ binds to NMDA and triggers a phosphotase (calcineurin) to dephosphorylate a protein and prevent binding to AMPA

what does LTD and LTP both require?

Ca2+. NMDA receptor activation

what is the basic circuit for memory in the hippocampus?

dentate granule cell → CA3 → CA1, stimulating the schaeffer collateral causes an EPSP in the CA1

what is the schaeffer collateral

axon between CA3 and CA1

what is the mechanism for long-term plasticity?

PKA activates CREB via phosphorylation which activates genes for long-term memory

CREB Gene 1 (ubiquitin hydroxylase)

degrades PKA and allows it to be active without serotonin

CREB Gene 2 (CPE)

causes structural changes in synapse

CREB Gene 3 (C/EBP)

enhances mRNA capacity and can be activated for long periods of time