Regulation of neurotransmitter release by endogenous nitric oxide in striatal slices

Taleen Hanania, Kenneth M. Johnson

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

This study sought to determine the potential role of nitric oxide (NO) in N-methyl-d-aspartate (NMDA)-stimulated efflux of [14C] γ-aminobutyric acid (GABA) and [3H]acetylcholine from striatal slices in vitro. In Mg2+-free buffer, NMDA-stimulated [14C]GABA and [3H]acetylcholine release were inhibited by the guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and, to a lesser extent, by the nitric oxide synthase inhibitor, nitroarginine (N-Arg). Since reversal of catecholamine transporters previously has been implicated in the mechanism underlying NO-induced catecholamine release, we used the GABA transport inhibitor, 1-(2-(((diphenylmethylene)imino)oxy)ethyl)-1,2,5,6-tetrahydro-3-pyridine-carboxylic acid hydrochloride (NNC-711), to address the role of GABA transport in NArg-sensitive NMDA-induced release. NNC-711 inhibited NMDA-stimulated [14C]GABA efflux by 50%, confirming our previous report that NMDA-stimulated GABA release is partially dependent on reversal of the transporter. The effect of N-Arg in the presence of NNC-711 was similar to its effect in the absence of the transport inhibitor, suggesting that reversal of the transporter is not involved in the NO component of NMDA-stimulated [14C]GABA release. These data suggest that glutamatergic transmission through striatal NMDA receptors is partially mediated through activation of the NO/guanylate cyclase pathway and that this mechanism may contribute to the tetrodotoxin sensitivity of NMDA-induced release of GABA and acetylcholine in the striatum. Copyright (C) 1998 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)111-117
Number of pages7
JournalEuropean Journal of Pharmacology
Volume359
Issue number2-3
DOIs
StatePublished - Oct 23 1998

Fingerprint

Corpus Striatum
gamma-Aminobutyric Acid
Neurotransmitter Agents
Aspartic Acid
Nitric Oxide
Acetylcholine
Guanylate Cyclase
Nitroarginine
Catecholamines
Aminobutyrates
Tetrodotoxin
Carboxylic Acids
Nitric Oxide Synthase
Buffers

Keywords

  • Acetylcholine release
  • GABA (γ-aminobutyric acid) release
  • Nitric oxide (NO)
  • NMDA receptor
  • Striatum

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Regulation of neurotransmitter release by endogenous nitric oxide in striatal slices. / Hanania, Taleen; Johnson, Kenneth M.

In: European Journal of Pharmacology, Vol. 359, No. 2-3, 23.10.1998, p. 111-117.

Research output: Contribution to journalArticle

Hanania, Taleen ; Johnson, Kenneth M. / Regulation of neurotransmitter release by endogenous nitric oxide in striatal slices. In: European Journal of Pharmacology. 1998 ; Vol. 359, No. 2-3. pp. 111-117.
@article{f954cdaa5bf440b696eb9b32fb525bbe,
title = "Regulation of neurotransmitter release by endogenous nitric oxide in striatal slices",
abstract = "This study sought to determine the potential role of nitric oxide (NO) in N-methyl-d-aspartate (NMDA)-stimulated efflux of [14C] γ-aminobutyric acid (GABA) and [3H]acetylcholine from striatal slices in vitro. In Mg2+-free buffer, NMDA-stimulated [14C]GABA and [3H]acetylcholine release were inhibited by the guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and, to a lesser extent, by the nitric oxide synthase inhibitor, nitroarginine (N-Arg). Since reversal of catecholamine transporters previously has been implicated in the mechanism underlying NO-induced catecholamine release, we used the GABA transport inhibitor, 1-(2-(((diphenylmethylene)imino)oxy)ethyl)-1,2,5,6-tetrahydro-3-pyridine-carboxylic acid hydrochloride (NNC-711), to address the role of GABA transport in NArg-sensitive NMDA-induced release. NNC-711 inhibited NMDA-stimulated [14C]GABA efflux by 50{\%}, confirming our previous report that NMDA-stimulated GABA release is partially dependent on reversal of the transporter. The effect of N-Arg in the presence of NNC-711 was similar to its effect in the absence of the transport inhibitor, suggesting that reversal of the transporter is not involved in the NO component of NMDA-stimulated [14C]GABA release. These data suggest that glutamatergic transmission through striatal NMDA receptors is partially mediated through activation of the NO/guanylate cyclase pathway and that this mechanism may contribute to the tetrodotoxin sensitivity of NMDA-induced release of GABA and acetylcholine in the striatum. Copyright (C) 1998 Elsevier Science B.V.",
keywords = "Acetylcholine release, GABA (γ-aminobutyric acid) release, Nitric oxide (NO), NMDA receptor, Striatum",
author = "Taleen Hanania and Johnson, {Kenneth M.}",
year = "1998",
month = "10",
day = "23",
doi = "10.1016/S0014-2999(98)00636-0",
language = "English (US)",
volume = "359",
pages = "111--117",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - Regulation of neurotransmitter release by endogenous nitric oxide in striatal slices

AU - Hanania, Taleen

AU - Johnson, Kenneth M.

PY - 1998/10/23

Y1 - 1998/10/23

N2 - This study sought to determine the potential role of nitric oxide (NO) in N-methyl-d-aspartate (NMDA)-stimulated efflux of [14C] γ-aminobutyric acid (GABA) and [3H]acetylcholine from striatal slices in vitro. In Mg2+-free buffer, NMDA-stimulated [14C]GABA and [3H]acetylcholine release were inhibited by the guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and, to a lesser extent, by the nitric oxide synthase inhibitor, nitroarginine (N-Arg). Since reversal of catecholamine transporters previously has been implicated in the mechanism underlying NO-induced catecholamine release, we used the GABA transport inhibitor, 1-(2-(((diphenylmethylene)imino)oxy)ethyl)-1,2,5,6-tetrahydro-3-pyridine-carboxylic acid hydrochloride (NNC-711), to address the role of GABA transport in NArg-sensitive NMDA-induced release. NNC-711 inhibited NMDA-stimulated [14C]GABA efflux by 50%, confirming our previous report that NMDA-stimulated GABA release is partially dependent on reversal of the transporter. The effect of N-Arg in the presence of NNC-711 was similar to its effect in the absence of the transport inhibitor, suggesting that reversal of the transporter is not involved in the NO component of NMDA-stimulated [14C]GABA release. These data suggest that glutamatergic transmission through striatal NMDA receptors is partially mediated through activation of the NO/guanylate cyclase pathway and that this mechanism may contribute to the tetrodotoxin sensitivity of NMDA-induced release of GABA and acetylcholine in the striatum. Copyright (C) 1998 Elsevier Science B.V.

AB - This study sought to determine the potential role of nitric oxide (NO) in N-methyl-d-aspartate (NMDA)-stimulated efflux of [14C] γ-aminobutyric acid (GABA) and [3H]acetylcholine from striatal slices in vitro. In Mg2+-free buffer, NMDA-stimulated [14C]GABA and [3H]acetylcholine release were inhibited by the guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and, to a lesser extent, by the nitric oxide synthase inhibitor, nitroarginine (N-Arg). Since reversal of catecholamine transporters previously has been implicated in the mechanism underlying NO-induced catecholamine release, we used the GABA transport inhibitor, 1-(2-(((diphenylmethylene)imino)oxy)ethyl)-1,2,5,6-tetrahydro-3-pyridine-carboxylic acid hydrochloride (NNC-711), to address the role of GABA transport in NArg-sensitive NMDA-induced release. NNC-711 inhibited NMDA-stimulated [14C]GABA efflux by 50%, confirming our previous report that NMDA-stimulated GABA release is partially dependent on reversal of the transporter. The effect of N-Arg in the presence of NNC-711 was similar to its effect in the absence of the transport inhibitor, suggesting that reversal of the transporter is not involved in the NO component of NMDA-stimulated [14C]GABA release. These data suggest that glutamatergic transmission through striatal NMDA receptors is partially mediated through activation of the NO/guanylate cyclase pathway and that this mechanism may contribute to the tetrodotoxin sensitivity of NMDA-induced release of GABA and acetylcholine in the striatum. Copyright (C) 1998 Elsevier Science B.V.

KW - Acetylcholine release

KW - GABA (γ-aminobutyric acid) release

KW - Nitric oxide (NO)

KW - NMDA receptor

KW - Striatum

UR - http://www.scopus.com/inward/record.url?scp=0032561187&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032561187&partnerID=8YFLogxK

U2 - 10.1016/S0014-2999(98)00636-0

DO - 10.1016/S0014-2999(98)00636-0

M3 - Article

VL - 359

SP - 111

EP - 117

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 2-3

ER -