Blockade of N- and Q-type Ca2+ channels inhibit K+-evoked [3H]acetylcholine release in rat hippocampal slices

In the present study, we examined the contribution of specific Ca2+ channels to K(+)-evoked hippocampal acetylcholine (ACh) release using [3H]choline loaded hippocampal slices. [3H]ACh release was Ca(2+)-dependent, blocked by the nonspecific Ca2+ channel blocker verapamil, but not by blockade of L-t...

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Bibliographic Details
Published in:Brain research bulletin 1996, Vol.40 (4), p.283-286
Main Authors: SAYDOFF, J. A, ZACZEK, R
Format: Article
Language:English
Subjects:
Acetylcholine - metabolism
Analysis of Variance
Animals
Biological and medical sciences
Calcium Channel Blockers - pharmacology
Central nervous system
Central neurotransmission. Neuromudulation. Pathways and receptors
Fundamental and applied biological sciences. Psychology
Hippocampus - drug effects
Hippocampus - metabolism
In Vitro Techniques
Male
Potassium - pharmacology
Rats
Rats, Wistar
Tritium
Vertebrates: nervous system and sense organs
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Summary:In the present study, we examined the contribution of specific Ca2+ channels to K(+)-evoked hippocampal acetylcholine (ACh) release using [3H]choline loaded hippocampal slices. [3H]ACh release was Ca(2+)-dependent, blocked by the nonspecific Ca2+ channel blocker verapamil, but not by blockade of L-type Ca2+ channels. The N-type Ca2+ channel blocker omega-conotoxin GVIA (omega-CgTx GVIA; 250 nM) inhibited [3H]ACh release by 44% and the P/Q-type Ca2+ channel blocker omega-agatoxin IVA (omega-Aga IVA; 400 nM) inhibited [3H]ACh release by 27%, with the combination resulting in a nearly additive 79% inhibition. Four hundred or one thousand nM omega-Aga IVA was necessary to inhibit [3H]ACh release. omega-Conotoxin MVIIC (omega-CTx-MVIIC) was used after first blocking N-type Ca2+ channels with omega-CgTx GVIA (1 microM). Under these conditions, 500 nM omega-CTx-MVIIC led to a nearly maximal inhibition of the omega-CgTx GVIA-insensitive [3H]ACh release. Based on earlier reports about the relative sensitivity of cloned and native Ca2+ channels to these toxins, this study indicates that N- and Q-type Ca2+ channels primarily mediate K(+)-evoked hippocampal [3H]ACh release.
ISSN:0361-9230
1873-2747
DOI:10.1016/0361-9230(96)00071-8