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

Area of Science:

• Neuroscience
• Synaptic Plasticity
• Auditory System Development

Background:

• Posttetanic potentiation (PTP) is a short-term synaptic plasticity phenomenon.
• PTP duration lasts tens of seconds following high-frequency stimulation.
• Protein kinase C (PKC) is implicated in mediating PTP.

Purpose of the Study:

• To investigate the distinct mechanisms of PTP at the calyx of Held synapse before and after hearing onset.
• To elucidate the differential roles of PKC isoforms in mediating PTP.
• To understand the functional consequences of these mechanistic differences.

Main Methods:

• Electrophysiological recordings at the calyx of Held synapse.
• High-frequency stimulation protocols to induce PTP.
• Pharmacological and genetic manipulations to assess PKC isoform function (e.g., viral expression).

Main Results:

• PTP is mediated by increased release probability (p) before hearing onset and increased readily releasable pool (RRP) after hearing onset.
• PKCγ and PKCβ isoforms exhibit differential actions.
• PKCγ increases p before hearing onset, while PKCβ increases RRP after hearing onset.
• PKCγ can override PKCβ to increase p even in hearing animals.

Conclusions:

• Two closely related PKC isoforms, PKCγ and PKCβ, mediate PTP through distinct mechanisms.
• The mechanism of PTP shifts from release probability to readily releasable pool with hearing onset.
• Differential actions of PKC isoforms contribute to developmental changes in synaptic plasticity.