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

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 flu...

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Bibliographic Details
Published in:Brain research 2005-11, Vol.1063 (1), p.9-14
Main Authors: Petzold, Gabor C., Scheibe, Franziska, Braun, Johann S., Freyer, Dorette, Priller, Josef, Dirnagl, Ulrich, Dreier, Jens P.
Format: Article
Language:English
Subjects:
Action Potentials - physiology
Animals
Biological and medical sciences
Calcium - metabolism
Calcium Channels, P-Type - metabolism
Calcium Channels, Q-Type - metabolism
Cell culture
Cells, Cultured
Central nervous system
Central neurotransmission. Neuromudulation. Pathways and receptors
Excitotoxicity
Extracellular Fluid - physiology
Fundamental and applied biological sciences. Psychology
Intracellular Fluid - metabolism
N-methyl- d-aspartate receptor
Neocortex
Neocortex - cytology
Neocortex - metabolism
Neurons - cytology
Neurons - metabolism
Nitric oxide
Nitric Oxide - physiology
Rats
Receptors, N-Methyl-D-Aspartate - metabolism
Signal Transduction - physiology
Vertebrates: nervous system and sense organs
Voltage-gated calcium channel
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Summary: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 ([Ca 2+] i). The potassium-induced [Ca 2+] 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.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2005.09.048