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Effects of Calcium Channel Antagonists on Calcium Entry and Glutamate Release from Cultured Rat Cerebellar Granule Cells
Author(s) -
Graham Margaret E.,
Burgoyne Robert D.
Publication year - 1995
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.1471-4159.1995.65062517.x
Subject(s) - granule (geology) , calcium , glutamate receptor , calcium channel , chemistry , cerebellum , p type calcium channel , biophysics , t type calcium channel , neuroscience , biology , biochemistry , receptor , organic chemistry , paleontology
Using a range of Ca 2+ channel blockers we have investigated the Ca 2+ channel subtypes that mediate the depolarisation‐induced elevation of the intracellular free Ca 2+ concentration ([Ca 2+ ] i ) and glutamate release from cultured rat cerebellar granule cells. ω‐Conotoxin‐GVIA had little effect on either the transient or plateau phase of the depolarisation‐induced [Ca 2+ ] i rise or on glutamate release, ruling out a significant role for N‐type Ca 2+ channels. Nifedipine substantially inhibited the initial transient rise in [Ca 2+ ] i and the plateau phase of the [Ca 2+ ] i rise and glutamate release, suggesting the involvement of L‐type Ca 2+ channels. Both ω‐agatoxin and ω‐conotoxin‐MVIIC also inhibited the transient rise in [Ca 2+ ] i and glutamate release but not the plateau phase of the [Ca 2+ ] i rise. The inhibitions by nifedipine were not increased by coaddition of ω‐conotoxin‐MVIIC, suggesting overlapping sensitivity to these channel blockers. These data show that glutamate release from granule cells in response to depolarisation with a high KCI level involves Ca 2+ currents that are sensitive to nifedipine, ω‐agatoxin‐IVA, and also ω‐conotoxin‐MVIIC. The overlapping sensitivity of the channels to these toxins prevents attribution of any of the phases of the [Ca 2+ ] i rise or glutamate release to distinct P‐, Q‐, or O‐type Ca 2+ currents.