Potentiation of transmitter release by protein kinase C in goldfish retinal bipolar cells
Potentiation of transmitter release by protein kinase C in goldfish retinal bipolar cells
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DOI:
10.1111/j.1469-7793.1998.219bf.x
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发表时间:
1998-10-01
影响因子:
5.5
通讯作者:
Tachibana, M
中科院分区:
文献类型:
--
作者:
Minami, N;Berglund, K;Tachibana, M
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, 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 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.