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NMDA receptor activation induces glutamate release through nitric oxide synthesis in guinea pig dentate gyrus.
Brain Res. 1996 Jul 22; 728(1):105-10.BR

Abstract

We tested the hypothesis that the release of glutamate following activation of N-methyl-D-aspartate (NMDA) receptors is mediated by nitric oxide (NO) production, using slices of the guinea pig hippocampus. The NMDA-induced glutamate release from slices of dentate gyrus or CA1, which was both concentration-dependent and Ca(2+)-dependent, was also Mg(2+)-sensitive and abolished by MK-801, a selective non-competitive NMDA receptor antagonist. In dentate gyrus, the NMDA-induced glutamate release was inhibited non-significantly by tetrodotoxin, whereas the NO synthase (NOS) inhibitor NG-nitro-L-arginine (L-NNA) blocked the NMDA-induced release of glutamate in a concentration-dependent manner, but not a high K(+)-evoked release of glutamate. In addition, the L-NNA blockade of NMDA-induced release of glutamate was recovered by pretreatment with L-arginine, the normal substrate for NOS. These results suggest that activation of NMDA receptors in dentate gyrus, as well as subsequent Ca2+ fluxes, is required for the neuronal glutamate release mediated by NO production. On the other hand, the NMDA-evoked glutamate release from CA1 region was tetrodotoxin-sensitive and was not inhibited by L-NNA, thereby suggesting that activation of NMDA receptors in CA1 results in increased glutamate release in an NO-independent manner. Taken together, the NMDA receptor-mediated neuronal release of glutamate from the guinea pig dentate gyrus likely involves the recruitment of NOS activity.

Authors+Show Affiliations

Department of Pharmacology, Kobe University School of Medicine, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8864303

Citation

Nei, K, et al. "NMDA Receptor Activation Induces Glutamate Release Through Nitric Oxide Synthesis in Guinea Pig Dentate Gyrus." Brain Research, vol. 728, no. 1, 1996, pp. 105-10.
Nei K, Matsuyama S, Shuntoh H, et al. NMDA receptor activation induces glutamate release through nitric oxide synthesis in guinea pig dentate gyrus. Brain Res. 1996;728(1):105-10.
Nei, K., Matsuyama, S., Shuntoh, H., & Tanaka, C. (1996). NMDA receptor activation induces glutamate release through nitric oxide synthesis in guinea pig dentate gyrus. Brain Research, 728(1), 105-10.
Nei K, et al. NMDA Receptor Activation Induces Glutamate Release Through Nitric Oxide Synthesis in Guinea Pig Dentate Gyrus. Brain Res. 1996 Jul 22;728(1):105-10. PubMed PMID: 8864303.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NMDA receptor activation induces glutamate release through nitric oxide synthesis in guinea pig dentate gyrus. AU - Nei,K, AU - Matsuyama,S, AU - Shuntoh,H, AU - Tanaka,C, PY - 1996/7/22/pubmed PY - 1996/7/22/medline PY - 1996/7/22/entrez SP - 105 EP - 10 JF - Brain research JO - Brain Res VL - 728 IS - 1 N2 - We tested the hypothesis that the release of glutamate following activation of N-methyl-D-aspartate (NMDA) receptors is mediated by nitric oxide (NO) production, using slices of the guinea pig hippocampus. The NMDA-induced glutamate release from slices of dentate gyrus or CA1, which was both concentration-dependent and Ca(2+)-dependent, was also Mg(2+)-sensitive and abolished by MK-801, a selective non-competitive NMDA receptor antagonist. In dentate gyrus, the NMDA-induced glutamate release was inhibited non-significantly by tetrodotoxin, whereas the NO synthase (NOS) inhibitor NG-nitro-L-arginine (L-NNA) blocked the NMDA-induced release of glutamate in a concentration-dependent manner, but not a high K(+)-evoked release of glutamate. In addition, the L-NNA blockade of NMDA-induced release of glutamate was recovered by pretreatment with L-arginine, the normal substrate for NOS. These results suggest that activation of NMDA receptors in dentate gyrus, as well as subsequent Ca2+ fluxes, is required for the neuronal glutamate release mediated by NO production. On the other hand, the NMDA-evoked glutamate release from CA1 region was tetrodotoxin-sensitive and was not inhibited by L-NNA, thereby suggesting that activation of NMDA receptors in CA1 results in increased glutamate release in an NO-independent manner. Taken together, the NMDA receptor-mediated neuronal release of glutamate from the guinea pig dentate gyrus likely involves the recruitment of NOS activity. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/8864303/NMDA_receptor_activation_induces_glutamate_release_through_nitric_oxide_synthesis_in_guinea_pig_dentate_gyrus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/0006-8993(96)00394-0 DB - PRIME DP - Unbound Medicine ER -