Role of Nitric Oxide in Central Synaptic Transmission: Effects on Neurotransmitter Release
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概要
- 論文の詳細を見る
Nitric oxide (NO), an unstable radical formed via oxidative deamination of L-arginine by NO synthase, has the activity to evoke release of several neurotransmitters including acetylcholine, catechol-amines and neuroactive amino acids. <I>N</I>-methyl-D-aspartate (NMDA) receptor stimulation also causes neurotransmitter release through NO formation, which is supported by the data that extracellular hemoglobin ompletely abolishes the stimulatory effect of NMDA on neurotransmitter release. In addition, NO formed by NMDA receptor activation exhibits its stimulatory action on neurotransmitter release extracellularly. A product formed by the reaction of NO and superoxide, peroxynitrite, is also considered to be partly involved in NO-evoked neurotransmitter release. The removal of Ca<SUP>2+</SUP> or Na<SUP>+</SUP> significantly reduces the release of GABA evoked by an NO generator, S-nitroso-<I>N</I>-acetylpenicillamine (SNAP), and simultaneous withdrawal of these ions completely abolishes the SNAP-induced release of GABA. Either in the presence or absence of Ca<SUP>2+</SUP>, GABA transport inhibitors such as nipecotic acid dose-dependently suppress the SNAP-induced GABA release in the presence of Na<SUP>+</SUP>. These results indicate that NO-evoked neurotransmitter release is mediated by two distinct release systems, a Ca<SUP>2+</SUP>-dependent system and the reverse process of a Na<SUP>+</SUP>-dependent carrier-mediated transport system.
- 社団法人 日本薬理学会の論文
- 1995-09-01
著者
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OHKUMA Seitaro
Department of Pharmacology, Kawasaki Medical School
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Ohkuma Seitaro
Department Of Pharmacology Kawasaki Medical School
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Ohkuma S
Department Of Pharmacology Kyoto Prefetural University Of Medicine
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Kuriyama Kinya
Department Of Health Promoting Acupuncture And Moxibution Meiji University Of Oriental Medicine
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Kuriyama K
Department Of Pharmacology Kyoto Prefectural University Of Medicine
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