Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse.

Neurons dynamically regulate neurotransmitter release through many processes known collectively as synaptic plasticity. Post-tetanic potentiation (PTP) is a widespread form of synaptic plasticity that lasts for tens of seconds that may have important computational roles and contribute to short-term memory. According to a leading mechanism, presynaptic calcium activates protein kinase C (PKC) to increase neurotransmitter release. Pharmacological studies have also implicated this mechanism at hippocampal CA3 to CA1 synapses, but there are concerns about the specificity of PKC activators and inhibitors. We therefore used a molecular genetic approach and found that PTP was unaffected when all calcium-dependent PKC isozymes were eliminated. We conclude that PKC isozymes are not the calcium sensors that mediate PTP at the CA3 to CA1 synapse.