Voltage-dependent calcium channel involvement in NMDA-induced activation of NOS

Sudarkodi Alagarsamy, Kenneth M. Johnson

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

We have previously shown that N-methyl-D-aspartate (NMDA) increases nitric oxide synthase (NOS) activity in rat frontal cortex; however, the actual mechanism of this activation has not been addressed. Tetrodotoxin (TTX; 0.05 µM) inhibited NMDA-activated NOS, suggesting that TTX-sensitive Na+ channels are interposed between the NMDA receptors and the NOS cellular compartment. The NMDA response was also blocked by voltage-dependent Ca2+ channel (VDCC) blockers including Cd2+, Co2+, funnel web spider toxin (FTX) and w-Aga IVa, but not by nifedipine or w-conotoxin. These data suggest that Ca2+ flux through P- and/or Q-type VDCC subsequent to NMDA-induced depolarization may be at least as important for NOS activation as Ca2+ entry through the NMDA receptor.

Original languageEnglish (US)
Pages (from-to)2250-2254
Number of pages5
JournalNeuroReport
Volume6
Issue number16
DOIs
StatePublished - Nov 1995

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Keywords

  • Aga IVa toxin
  • Cortex
  • Glutamate
  • L-methyl-D-aspartate (NMDA)
  • P-type calcium channel
  • Receptor binding

ASJC Scopus subject areas

  • Neuroscience(all)

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