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Modulation of voltage‐dependent calcium current in Helix aspersa buccal neurones by serotonin and protein kinase C activators
Author(s) -
Hill-Venning C,
Cottrell GA
Publication year - 1992
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1992.sp003656
Subject(s) - protein kinase c , okadaic acid , calcium , protein kinase a , excitatory postsynaptic potential , serotonin , biophysics , chemistry , biology , depolarization , medicine , microbiology and biotechnology , endocrinology , phosphatase , phosphorylation , biochemistry , inhibitory postsynaptic potential , receptor
In Helix aspersa, activation of the cerebral giant serotonin neurones (GSNs) evokes a biphasic, excitatory synaptic response in the M neurones of the buccal ganglia. Local application of serotonin to the current‐clamped M neurones also evokes fast and slow depolarizing responses. The slow response is thought to be dependent on calcium ions, whereas sodium ions have been implicated in the fast response. Here we provide further evidence that the slow response results from an increase in conductance to calcium ions, and show that okadaic acid, an antagonist of protein phosphatases 1 and 2A, potentiates the effect of serotonin, suggesting that the response is phosphorylation dependent. Further, agents known to activate protein kinase C, such as 1‐oleoyl‐2‐acetyl‐rac‐glycerol and active phorbol esters (but not an inactive one) were found to increase the calcium current (actually carried by barium ions) of the M neurones. Such data suggest that the slow synaptic response mediated by serotonin can occur by activation of protein kinase C and phosphorylation of the affected voltage‐sensitive calcium channels, or some closely associated protein(s).