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Rapid Communication: The Role of P‐Type Calcium Channels in the Depolarization‐Induced Activation of Nitric Oxide Synthase in Frontal Cortex
Author(s) -
Alagarsamy Sudarkodi,
Lonart Gyorgy,
Johnson Kenneth M.
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.1471-4159.1994.62010400.x
Subject(s) - nitric oxide synthase , depolarization , nitric oxide , neuroscience , chemistry , biophysics , calcium , frontal cortex , biology , organic chemistry
In this study we demonstrate that 50 mRS K + stimulates the conversion of L‐[ 3 H] arginine to L‐[ 3 H] citrulline and that this effect is blocked by 10 μ M AT‐nitro‐ l ‐arginine, a nitric oxide synthase inhibitor, and Ca 2+ ‐free conditions. Amiloride (1 m M ) and low Na + conditions were used to test the possible involvement of the Na + ‐Ca 2+ exchanger. These treatments were without effect. The calcium channel blockers 10 mRS Mg 2+ , 100 μ M Cd 2+ , and 10 mRS Co 2+ also blocked the K + response, suggesting the involvement of voltage‐dependent calcium channels (VDCCs). The specific VDCC involved seems to be the P type, as funnel‐web spider toxin blocked the response whereas 200 μ M Ni 2+ , 10 μ M nifedipine, and 100 n M ω‐conotoxin did not.