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Relationship of Dihydropyridine Binding Sites with Calcium‐Dependent Neurotransmitter Release in Synaptosomes
Author(s) -
Massieu Lourdes,
Tapia Ricardo
Publication year - 1988
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 - 10.1111/j.1471-4159.1988.tb03085.x
Subject(s) - nitrendipine , chemistry , nifedipine , synaptosome , neurotransmitter , calcium , dihydropyridine , potassium , ruthenium red , pharmacology , biophysics , endocrinology , biochemistry , receptor , biology , organic chemistry
In the present work, we have studied the effect of ruthenium red (RuR), La 3+ , and 4‐aminopyridine (4‐AP) on the specific binding of (+)‐[ 3 H]PN200–110 to synaptosomes, as well as the effect of nitrendipine, nifedipine, and BAY K. 8644 on γ‐[ 3 H]aminobutyric acid ([ 3 H]GABA) release induced by potassium depolarization and by 4‐AP in synaptosomes. Scatchard plots indicated that neither RuR nor 4‐AP modifies the K D and B max of [ 3 H]PN200–110 specific binding, whereas La 3+ decreased the B max by about 25%; when the effect of the drugs on the total binding of PN200–110 was studied, a similar inhibition by La 3+ was found. The calcium antagonists, nitrendipine and nifedipine, did not affect at all the potassium‐stimulated release of [ 3 H]GABA nor its release induced by 4‐AP. The calcium agonist BAY K 8644 failed to affect both the spontaneous and the potassium‐stimulated GABA release. Our results suggest that the binding sites of dihydropyridines in presynaptic membranes are not related to the calcium channels involved in neurotransmitter release with which RuR, La 3+ , and 4‐AP interact.