Purves Ch8
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8 terms
Terms | Definitions |
|---|---|
 Synaptic facilitation | is a rapid increase in synaptic strength that occurs when two or more action potentials invade the presynaptic terminal within a few milliseconds of each other. By varying the time interval between presynaptic action potentials, it can be seen that facilitation lasts for tens of milliseconds. |
| What causes facilitation? | Prolonged elevation of presynaptic calcium levels following an action potential. |
| What causes synaptic depression? | progressive depletion of a pool of synaptic vesicles that are available for release. |
| What's the difference between augmentation and potentiation? | While augmentation rises and falls over a few seconds, potentiation acts over a time scale of tens of seconds to minutes. As a result of its slower time course, potentiation can greatly outlast the tetanus. |
| What protein does augmentation rely on and how does it operate? | Augmentation depends on the priming protein, munc13, apecifically, isoform 2 of munc13. It increases the releasable pool size. |
| What forms of short term plasticity is synapsin implicated in? | Synaptic depression depends of the kinetics of synapsin and the depletion of the ready pool. Potentiation involves enhanced presynaptic Ca2+ --> activates protein kinases that phosphorylate proteins, like synapsin, that regulate transmitter release. |
| Describe the sensitization pathway of the gill withdraw reflex in Aplysia | tail shock --> excites sensory neurons --> excites modulatory interneuron --> releases serotonin on the presynaptic terminals, on the sensory neurons of the siphon --> Serotonin binds to a G-protein coupled receptor --> production of cAMP --> cAMP binds regulatory subunits of protein kinase A (PKA), liberating its catalytic units --> PKA phosphorylates many proteins, including K+ channels --> Prolonged action potential --> More calcium --> More NT release. |
| Describe the long-term sensitization pathway of Aplysia | Relies on the same mechanism as short-term, but with repeated training (i.e., additional tail shocks), the serotonin-activated PKA involved in short-term sensitization now also phosphorylates—and thereby activates—the transcriptional activator CREB. CREB binding to the cAMP responsive elements (CREs) in regulatory regions of nuclear DNA increases the rate of transcription of downstream genes. consequences gene been identified. CREB stimulates the synthesis of an enzyme, ubiquitin hydroxylase, that stimulates degradation of the regulatory subunit of PKA. This causes a persistent increase in the amount of free catalytic subunit, meaning that some PKA is persistently active and no longer requires serotonin to be activated. CREB also stimulates another transcriptional activator protein, called C/EBP. C/EBP stimulates transcription of other, unknown genes that cause addition of synaptic terminals, yielding a long-term increase in the number of synapses between the sensory and the motor neurons. |
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