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The Journal of Neuroscience, September 1, 1999, 19(17):7262-7267

Presynaptic Mechanism for Phorbol Ester-Induced Synaptic Potentiation

Tetsuya Hori¹, Yoshimi Takai², and Tomoyuki Takahashi¹

¹ Department of Neurophysiology, University of Tokyo Faculty of Medicine, Tokyo 113-0033 Japan, and ² Department of Molecular Biology and Biochemistry, Osaka University Medical School, Suita 565-0871 Japan

Phorbol ester facilitates transmitter release at a variety of synapses, and the phorbol ester-induced synaptic potentiation (PESP) is a model for presynaptic facilitation. To address the mechanism underlying PESP, we have made paired whole-cell recordings from the giant presynaptic terminal, the calyx of Held, and its postsynaptic target in the medial nucleus of the trapezoid body in rat brainstem slices. Phorbol ester potentiated EPSCs without affecting either presynaptic calcium currents or potassium currents. Protein kinase C inhibitors applied from outside or injected directly into the presynaptic terminal attenuated the PESP. Furthermore, presynaptic loading of a synthetic peptide with the sequence of the N-terminal domain of Doc2 interacting with Munc13-1 (Mid peptide) significantly attenuated PESP, whereas mutated Mid peptide had no effect. We conclude that the target of the presynaptic facilitatory effect of phorbol ester resides downstream of calcium influx and may involve both protein kinase C and Doc2 - Munc13-1 interaction.

Key words: phorbol ester; synaptic facilitation; Doc2; Munc13-1; protein kinase C; the calyx of Held; presynaptic recording

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19177262-06$05.00/0

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