POTENTIATION OF TRANSMITTER RELEASE BY PROTEIN-KINASE-C IN GOLDFISH RETINAL BIPOLAR CELLS

1. We examined whether transmitter release could be modified by the ac tivation of protein kinase C (PKC) of retinal bipolar cells. A bipolar cell with a large axon terminal was isolated from the goldfish retina . The presynaptic Ca2+ current was measured under whole-cell voltage c lamp, and the released transmitter (probably glutamate) was detected e lectrophysiologically by using the response of NMDA receptors of catfi sh horizontal cells as a reporter. 2. Transmitter release was potentia ted by a PKC activator, phorbol 12-myristate 13-acetate (PMA), but not by an ineffective phorbol ester, 4 alpha-phorbol 12,13-didecanoate. A PKC inhibitor, bisindolylmaleimide I, did not affect the transmitter release by itself but blocked the PMA-induced potentiation of transmit ter release. These results suggest that the actions of PMA were mediat ed via the activation of PKC. 3. Introduction of 5 mM EGTA into the pr esynaptic terminals of bipolar cells revealed two separate components of transmitter release. A rapid component was triggered immediately af ter depolarization while a slow component appeared with a delay. Appli cation of PMA selectively potentiated the slow component without affec ting the Ca2+ dependence of exocytosis. 4. We suggest that the activat ion of PKC may modify the recruitment process of synaptic vesicles in retinal bipolar cells.