The effects of dihydropyridines of neurotransmitter release from cultured neuronal cells

Ismail A. Shalaby; Sathapana Kongsamut; Stephen B. Freedman; Richard J. Miller

doi:10.1016/0024-3205(84)90100-0

The effects of dihydropyridines of neurotransmitter release from cultured neuronal cells

Ismail A. Shalaby, Sathapana Kongsamut, Stephen B. Freedman, Richard J. Miller^*

^*Corresponding author for this work

Pharmacology

Research output: Contribution to journal › Article › peer-review

36 Scopus citations

Abstract

Depolarizing stimuli increase the release of transmitter substances from cultured PC12 pheochromocytoma cells and reaggregate cultures of mouse mesencephalic dopamine neurones. We measured the stimulated release of (³H) norepinephrine and (³H) dopamine from these systems respectively. In the cultured mouse dopaminergic neurones, several organic calcium channel blockers including nitrendipine, D-600, verapamil and diltiazem were unable to inhibit potassium-evoked transmitter release. However, release was blocked by 3 mM cobalt. The novel dihydropyridine calcium channel agonist BAY K8644 also had no effect on basal or evoked dopamine release. In contrast, BAY K8644 greatly stimulated the potassium-evoked release of (³H) norepinephrine from PC12 cells. The BAY K8644 enhanced release could be blocked by the dihydropyridine antagonist nitrendipine. These results indicate that while stimulus-secretion coupling in the PC12 cell line involves dihydropyridine sensitive calcium channels, this is not the case in primary cultured neurones.

Original language	English (US)
Pages (from-to)	1289-1295
Number of pages	7
Journal	Life Sciences
Volume	35
Issue number	12
DOIs	https://doi.org/10.1016/0024-3205(84)90100-0
State	Published - Sep 17 1984

Funding

The authors wish to thank Drs. Glyn Dawson, Mitchel Villereal and Alfred Helllleerr for the generous use of their tissue culture facilities and Della Akres forr preparation of the manuscript. This study was supported by NIH grants DA-,00221122 1 and DA-02575 to R.J.M. and MH-28942 to Alfred Heller. I.A.S. was a postdoctoral fellow of The National Hungtington's Disease Association. S.B.F. was a NATO (United Kingdom) Fellow. R.J.M. is an Alfred P. Sloan Fellow.

ASJC Scopus subject areas

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry, Genetics and Molecular Biology

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title = "The effects of dihydropyridines of neurotransmitter release from cultured neuronal cells",

abstract = "Depolarizing stimuli increase the release of transmitter substances from cultured PC12 pheochromocytoma cells and reaggregate cultures of mouse mesencephalic dopamine neurones. We measured the stimulated release of (3H) norepinephrine and (3H) dopamine from these systems respectively. In the cultured mouse dopaminergic neurones, several organic calcium channel blockers including nitrendipine, D-600, verapamil and diltiazem were unable to inhibit potassium-evoked transmitter release. However, release was blocked by 3 mM cobalt. The novel dihydropyridine calcium channel agonist BAY K8644 also had no effect on basal or evoked dopamine release. In contrast, BAY K8644 greatly stimulated the potassium-evoked release of (3H) norepinephrine from PC12 cells. The BAY K8644 enhanced release could be blocked by the dihydropyridine antagonist nitrendipine. These results indicate that while stimulus-secretion coupling in the PC12 cell line involves dihydropyridine sensitive calcium channels, this is not the case in primary cultured neurones.",

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note = "Funding Information: The authors wish to thank Drs. Glyn Dawson, Mitchel Villereal and Alfred Helllleerr for the generous use of their tissue culture facilities and Della Akres forr preparation of the manuscript. This study was supported by NIH grants DA-,00221122 1 and DA-02575 to R.J.M. and MH-28942 to Alfred Heller. I.A.S. was a postdoctoral fellow of The National Hungtington's Disease Association. S.B.F. was a NATO (United Kingdom) Fellow. R.J.M. is an Alfred P. Sloan Fellow.",

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N2 - Depolarizing stimuli increase the release of transmitter substances from cultured PC12 pheochromocytoma cells and reaggregate cultures of mouse mesencephalic dopamine neurones. We measured the stimulated release of (3H) norepinephrine and (3H) dopamine from these systems respectively. In the cultured mouse dopaminergic neurones, several organic calcium channel blockers including nitrendipine, D-600, verapamil and diltiazem were unable to inhibit potassium-evoked transmitter release. However, release was blocked by 3 mM cobalt. The novel dihydropyridine calcium channel agonist BAY K8644 also had no effect on basal or evoked dopamine release. In contrast, BAY K8644 greatly stimulated the potassium-evoked release of (3H) norepinephrine from PC12 cells. The BAY K8644 enhanced release could be blocked by the dihydropyridine antagonist nitrendipine. These results indicate that while stimulus-secretion coupling in the PC12 cell line involves dihydropyridine sensitive calcium channels, this is not the case in primary cultured neurones.

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The effects of dihydropyridines of neurotransmitter release from cultured neuronal cells

Abstract

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