title: Potentiation of transmitter release by protein kinase C in goldfish retinal bipolar cells.
abstract: 1. We examined whether transmitter release could be modified by the activation 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 clamp, and the released transmitter (probably glutamate) was detected electrophysiologically by using the response of NMDA receptors of catfish horizontal cells as a reporter. 2. Transmitter release was potentiated by a PKC activator, phorbol 12-myristate 13-acetate (PMA), but not by an ineffective phorbol ester, 4alpha-phorbol 12,13-didecanoate. A PKC inhibitor, bisindolylmaleimide I, did not affect the transmitter release by itself but blocked the PMA-induced potentiation of transmitter release. These results suggest that the actions of PMA were mediated via the activation of PKC. 3. Introduction of 5 mM EGTA into the presynaptic terminals of bipolar cells revealed two separate components of transmitter release. A rapid component was triggered immediately after depolarization while a slow component appeared with a delay. Application of PMA selectively potentiated the slow component without affecting the Ca2+ dependence of exocytosis. 4. We suggest that the activation of PKC may modify the recruitment process of synaptic vesicles in retinal bipolar cells.
authors.affiliation: Department of Psychology, Graduate School of Humanities and Sociology, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Minami
authors.forename: K
authors.initials: K
authors.lastname: Berglund
authors.forename: T
authors.initials: T
authors.lastname: Sakaba
authors.forename: H
authors.initials: H
authors.lastname: Kohmoto
authors.forename: M
authors.initials: M
authors.lastname: Tachibana
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology; D015220:Calcium Channels / Q000502:physiology*; D004533:Egtazic Acid / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism*; D006054:Goldfish; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D010703:Phorbol Esters / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000502:physiology; D011493:Protein Kinase C / Q000378:metabolism*; D012160:Retina / Q000166:cytology / Q000502:physiology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D004791:Enzyme Inhibitors; D018377:Neurotransmitter Agents; D010703:Phorbol Esters; C008876:phorbol-12,13-didecanoate; D018698:Glutamic Acid; D004533:Egtazic Acid; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate