Different routes of Ca2+ influx in NMDA-mediated generation of nitric oxide and arachidonic acid

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Abstract

Nitric oxide and arachidonic acid act as inter- and intracellular messengers in the central nervous system. It is well known that the NMDA-mediated generation of nitric oxide and arachidonic acid is dependent on extracellular Ca2+. However, the role of voltage-dependent calcium channels (VDCCs) in this regard is poorly understood. We report here that NMDA-mediated nitric oxide production in striatal neuron cultures is blocked (80%) by the L-type VDCC antagonist nifedipine, but not by ω-conotoxin or co-agatoxin IVA, antagonists of the N- and P-type VDCCs respectively. By contrast, none of the VDCC antagonists inhibited the NMDA-mediated release of arachidonic acid. These data indicate that permeation through different Ca2+ channels is responsible for the production of arachidonic acid and nitric oxide in striatal neurons. © European Neuroscience Association.
Original languageEnglish
Pages (from-to)867-870
JournalEuropean Journal of Neuroscience
Volume9
DOIs
Publication statusPublished - 1 Jan 1997

Keywords

  • Channels
  • Glutamate
  • Mouse
  • Striatal neurons
  • cGMP

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