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Activation of protein kinase C by presynaptic FLRFamide receptors facilitates transmitter release at an aplysia cholinergic synapse.

Abstract：

:Modulation of evoked quantal transmitter release by protein kinase C (PKC) was investigated at an identified cholinergic neuro-neuronal synapse of the Aplysia buccal ganglion. Evoked acetylcholine release was increased by a diacylglycerol analog that activates PKC and was decreased by H-7, a blocker of PKC. FLRFamide facilitated evoked quantal release by increasing presynaptic Ca2+ influx. The inhibition of PKC by H-7 prevented both the increase of presynaptic Ca2+ influx and the facilitation of evoked acetylcholine release induced by the activation of presynaptic FLRFamide receptors. These results provide evidence that the activation of PKC could be a step in the intracellular pathway by which FLRFamide receptors increase evoked quantal acetylcholine release.

journal_name

Neuron

journal_title

Neuron

authors

Fossier P,Baux G,Tauc L

doi

10.1016/0896-6273(90)90087-v

subject

Has Abstract

pub_date

1990-10-01 00:00:00

pages

479-86

issue

4

eissn

0896-6273

issn

1097-4199

pii

0896-6273(90)90087-V

journal_volume

5

pub_type

杂志文章

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