Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.

ABSTRACT: 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 PKC? and PKC? are both present, PKC? mediates PTP by increasing p and partially suppressing PKC? actions. After hearing onset, PKC? is absent and PKC? produces PTP by increasing RRP. In hearing animals, virally expressed PKC? overrides PKC? to produce PTP by increasing p. Thus, two similar PKC isoforms mediate PTP in distinctly different ways.

SUBMITTER: Chu Y 

PROVIDER: S-EPMC4097165 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature