Short-term synaptic plasticity results from use-dependent activity, lasts on the timescale of milliseconds to minutes, and is thought to underlie working memory and neuronal information processing. Here, we focus on two forms of short-term plasticity: 1) post-tetanic potentiation (PTP), which is induced by high-frequency stimulation, and 2) presynaptic ionotropic receptor-activated synaptic enhancement, which can be produced by the activation of presynaptic glycine receptors. Potentiation of evoked and spontaneous responses is thought to arise from elevations in presynaptic residual Ca2+, which activates one or more molecular targets to increase neurotransmitter release. However, the Ca2+ sensor protein has not yet been identified. The overall goal of this work is to elucidate the Ca2+-dependent mechanisms of short-term plasticity.
| Identifer | oai:union.ndltd.org:harvard.edu/oai:dash.harvard.edu:1/12274616 |
| Date | 07 June 2014 |
| Creators | Chu, Yun |
| Contributors | Regehr, Wade G. |
| Publisher | Harvard University |
| Source Sets | Harvard University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis or Dissertation |
| Rights | open |
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