| First Author | Fioravante D | Year | 2011 |
| Journal | Neuron | Volume | 70 |
| Issue | 5 | Pages | 1005-19 |
| PubMed ID | 21658591 | Mgi Jnum | J:174964 |
| Mgi Id | MGI:5141567 | Doi | 10.1016/j.neuron.2011.04.019 |
| Citation | Fioravante D, et al. (2011) Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held. Neuron 70(5):1005-19 |
| abstractText | High-frequency stimulation leads to a transient increase in the amplitude of evoked synaptic transmission that is known as posttetanic potentiation (PTP). Here we examine the roles of the calcium-dependent protein kinase C isoforms PKCalpha and PKCbeta in PTP at the calyx of Held synapse. In PKCalpha/beta double knockouts, 80% of PTP is eliminated, whereas basal synaptic properties are unaffected. PKCalpha and PKCbeta produce PTP by increasing the size of the readily releasable pool of vesicles evoked by high-frequency stimulation and by increasing the fraction of this pool released by the first stimulus. PKCalpha and PKCbeta do not facilitate presynaptic calcium currents. The small PTP remaining in double knockouts is mediated partly by an increase in miniature excitatory postsynaptic current amplitude and partly by a mechanism involving myosin light chain kinase. These experiments establish that PKCalpha and PKCbeta are crucial for PTP and suggest that long-lasting presynaptic calcium increases produced by tetanic stimulation may activate these isoforms to produce PTP. |
