Nitric oxide modulates calcium entry through P/Q-type calcium channels and N-methyl-d-aspartate receptors in rat cortical neurons

Gabor C. Petzold, Franziska Scheibe, Johann S. Braun, Dorette Freyer, Josef Priller, Ulrich Dirnagl, Jens P. Dreier

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

Voltage-gated calcium channels (VGCC) and N-methyl-d-aspartate receptors (NMDAR) account for most of the depolarization-induced neuronal calcium entry. The susceptibility of individual routes of calcium entry for nitric oxide (NO) is largely unknown. We loaded cultured rat cortical neurons with fluo-4 acetoxymethylester to study the effect of the NO synthase inhibitor Nω-nitro-l-arginine and the NO donor S-nitroso-N-acetylpenicillamine on the intracellular calcium concentration ([Ca2+]i). The potassium-induced [Ca2+]i increase was amplified by Nω-nitro-l-arginine and attenuated by S-nitroso-N-acetylpenicillamine. This modulation was abolished by either the P/Q-type VGCC antagonist ω-agatoxin IVA or by the NMDAR antagonist MK-801, but not by N-type (ω-conotoxin GVIA) or L-type (nimodipine) VGCC blockers. These results suggest that NO can modulate neuronal calcium entry during depolarization by interacting with P/Q-type VGCC and NMDAR.

Original languageEnglish
Pages (from-to)9-14
Number of pages6
JournalBrain Research
Volume1063
Issue number1
DOIs
Publication statusPublished - Nov 23 2005

Keywords

  • Cell culture
  • Excitotoxicity
  • N-methyl-d-aspartate receptor
  • Neocortex
  • Nitric oxide
  • Voltage-gated calcium channel

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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