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Effects of Ion Channel Blockers and Phorbol Ester Treatments on [ 3 H]Dopamine Release and Neurotensin Facilitation of [ 3 H]Dopamine Release from Rat Mesencephalic Cells in Primary Culture
Author(s) -
Brouard Aline,
Pelaprat Didier,
Vial Micheline,
Lhiaubet AnneMarie,
Rostène William
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62041416.x
Subject(s) - protein kinase c , chemistry , endocrinology , medicine , dopamine , phorbol , veratridine , staurosporine , neurotensin , protein kinase a , channel blocker , amiloride , calcium , biophysics , biochemistry , biology , sodium , neuropeptide , receptor , sodium channel , phosphorylation , organic chemistry
In this work, we tested the effect of ion channel blockers and of phorbol ester treatments on [ 3 H]dopamine ([ 3 H]DA) release and neurotensin (NT)‐induced facilitation of [ 3 H]DA release from cultures of rat fetal mesencephalic cells. The potassium channel blockers tetraethylammonium and 4‐aminopyridine increased basal [ 3 H]DA release and decreased K + ‐evoked [ 3 H]DA release, whereas apamin was without effect. K + ‐evoked [ 3 H]DA release was decreased by ω‐conotoxin and nifedipine, totally suppressed by cadmium, and unaffected by amiloride. These results show the differential sensitivity of [ 3 H]DA release to blockade of various ion channels and suggest the involvement of N‐type, L‐type, and non‐L‐non‐N‐type, but not T‐type, voltage‐sensitive calcium channels in K + ‐evoked release. Phorbol 12‐myristate 13‐acetate increased both spontaneous and K + ‐evoked [ 3 H]DA release, suggesting a modulatory action of protein kinase C on DA release in this system. Unexpectedly, however, the effects of the phorbol ester were not counteracted by the protein kinase C inhibitors H7, staurosporine, or polymyxin B. NT‐induced facilitation of K + ‐evoked [ 3 H]DA release was insensitive to most of the ion channel blockers, except cadmium (64% decrease in NT effect), suggesting that the corresponding potassium' and calcium channels were not involved in the effect of NT on [ 3 H]DA release in this system. The NT effect was totally suppressed by phorbol ester treatments, indicating a possible desensitization of the corresponding transduction mechanisms after protein kinase C activation.