| First Author | Chu Y | Year | 2014 |
| Journal | Neuron | Volume | 82 |
| Issue | 4 | Pages | 859-71 |
| PubMed ID | 24794094 | Mgi Jnum | J:220910 |
| Mgi Id | MGI:5637456 | Doi | 10.1016/j.neuron.2014.04.003 |
| Citation | Chu Y, et al. (2014) Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity. Neuron 82(4):859-71 |
| abstractText | Posttetanic potentiation (PTP) is a widely observed form of short-term plasticity lasting for tens of seconds after high-frequency stimulation. Here we show that although protein kinase C (PKC) mediates PTP at the calyx of Held synapse in the auditory brainstem before and after hearing onset, PTP is produced primarily by an increased probability of release (p) before hearing onset, and by an increased readily releasable pool of vesicles (RRP) thereafter. We find that these mechanistic differences, which have distinct functional consequences, reflect unexpected differential actions of closely related calcium-dependent PKC isoforms. Prior to hearing onset, when PKCgamma and PKCbeta are both present, PKCgamma mediates PTP by increasing p and partially suppressing PKCbeta actions. After hearing onset, PKCgamma is absent and PKCbeta produces PTP by increasing RRP. In hearing animals, virally expressed PKCgamma overrides PKCbeta to produce PTP by increasing p. Thus, two similar PKC isoforms mediate PTP in distinctly different ways. |
