Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity
By Laura Busse, Alex R. Wade, Matteo Carandini. 2014
108 citations recorded by the source corpus.
Summary Post-tetanic 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 PKCγ and PKCβ are both present, PKCγ mediates PTP by increasing p and partially suppressing PKCβ actions. After hearing onset, PKCγ is absent and PKCβ produces PTP by increasing RRP. In hearing animals, virally expressed PKCγ overrides PKCβ to produce PTP by increasing p. Thus, two similar PKC isoforms mediate PTP in distinctly different ways.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Sensory Systems
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In Sensory Systems
Citations in the corpus
- Normalization as a canonical neural computation (2011, neutral): “This characterization of the responses of neural population”
- Primary Visual Cortex Represents the Difference Between Past and Present (2013, background): “component responses (Busse et al. 2009; MacEvoy et al. 2009), resulted in a significantly higher average contribution of 60% from the off-component, compared with 40% from the adaptive component (see Supplementary Table S4 for details).”