Nitric oxide-mediated excitatory effect on neurons of dorsal motor nucleus of vagus

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Abstract

The purpose of our study was to explore whether nitric oxide was involved as an intercellular messenger in the dorsal motor nucleus of the vagus (DMV). To achieve this purpose we examined DMV motoneurons of the rat in vitro with the use of the extracellular cell-attached recording technique. The motoneurons, in general, exhibit a spontaneous discharge and when exposed to NO-producing drugs (i.e., 3-300 μM L-arginine and 10-100 μM S-nitroso-N- acetylpenicillamine) exhibit a concentration-related increase in their spontaneous firing rate. Because NO activates soluble guanylate cyclase and increases guanosine 3',5'-cyclic monophosphate (cGMP), we tested dibutyryl- cGMP (30-300 μM) and found that it also excites DMV neurons. Perfusion of the DMV neurons with N(ω)-nitro-L-arginine (300 μM), an inhibitor of NO synthase (NOS), and with NO scavenger, reduced hemoglobin (1 μM), counteracted the excitatory effect of L-arginine and N-methyl-D-aspartate (NMDA). Perfusion of the preparation with LY-83583 (10 μM), an inhibitor of guanylate cyclase, also counteracted the effects of L-arginine and NMDA. These data indicate that NOS is present in DMV neurons, and that the excitatory effect of NMDA on these neurons is due in part to formation of NO and the resulting accumulation of cGMP in DMV neurons.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume266
Issue number1 29-1
StatePublished - 1994

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Motor Neurons
Nitric Oxide
Arginine
Neurons
N-Methylaspartate
Nitric Oxide Synthase
Hemoglobin M
6-anilino-5,8-quinolinedione
Perfusion
S-Nitroso-N-Acetylpenicillamine
Guanylate Cyclase
Cyclic GMP
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Physiology
  • Gastroenterology

Cite this

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abstract = "The purpose of our study was to explore whether nitric oxide was involved as an intercellular messenger in the dorsal motor nucleus of the vagus (DMV). To achieve this purpose we examined DMV motoneurons of the rat in vitro with the use of the extracellular cell-attached recording technique. The motoneurons, in general, exhibit a spontaneous discharge and when exposed to NO-producing drugs (i.e., 3-300 μM L-arginine and 10-100 μM S-nitroso-N- acetylpenicillamine) exhibit a concentration-related increase in their spontaneous firing rate. Because NO activates soluble guanylate cyclase and increases guanosine 3',5'-cyclic monophosphate (cGMP), we tested dibutyryl- cGMP (30-300 μM) and found that it also excites DMV neurons. Perfusion of the DMV neurons with N(ω)-nitro-L-arginine (300 μM), an inhibitor of NO synthase (NOS), and with NO scavenger, reduced hemoglobin (1 μM), counteracted the excitatory effect of L-arginine and N-methyl-D-aspartate (NMDA). Perfusion of the preparation with LY-83583 (10 μM), an inhibitor of guanylate cyclase, also counteracted the effects of L-arginine and NMDA. These data indicate that NOS is present in DMV neurons, and that the excitatory effect of NMDA on these neurons is due in part to formation of NO and the resulting accumulation of cGMP in DMV neurons.",
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