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

doi:10.1016/j.brainres.2005.09.048

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

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-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 language	English
Pages (from-to)	9-14
Number of pages	6
Journal	Brain Research
Volume	1063
Issue number	1
DOIs	https://doi.org/10.1016/j.brainres.2005.09.048
Publication status	Published - 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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10.1016/j.brainres.2005.09.048

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

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.",

keywords = "Cell culture, Excitotoxicity, N-methyl-d-aspartate receptor, Neocortex, Nitric oxide, Voltage-gated calcium channel",

author = "Petzold, {Gabor C.} and Franziska Scheibe and Braun, {Johann S.} and Dorette Freyer and Josef Priller and Ulrich Dirnagl and Dreier, {Jens P.}",

note = "Funding Information: This study was supported by grants from the Deutsche Forschungsgemeinschaft (SFB 507 to J.P., U.D., and J.P.D.; PE 1193/1-1 to G.C.P.) and by the Hermann and Lilly Schilling Foundation (U.D.).",

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doi = "10.1016/j.brainres.2005.09.048",

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T1 - Nitric oxide modulates calcium entry through P/Q-type calcium channels and N-methyl-d-aspartate receptors in rat cortical neurons

AU - Petzold, Gabor C.

AU - Scheibe, Franziska

AU - Braun, Johann S.

AU - Freyer, Dorette

AU - Priller, Josef

AU - Dirnagl, Ulrich

AU - Dreier, Jens P.

N1 - Funding Information: This study was supported by grants from the Deutsche Forschungsgemeinschaft (SFB 507 to J.P., U.D., and J.P.D.; PE 1193/1-1 to G.C.P.) and by the Hermann and Lilly Schilling Foundation (U.D.).

PY - 2005/11/23

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N2 - 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.

AB - 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.

KW - Cell culture

KW - Excitotoxicity

KW - N-methyl-d-aspartate receptor

KW - Neocortex

KW - Nitric oxide

KW - Voltage-gated calcium channel

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

Abstract

Keywords

ASJC Scopus subject areas

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