Suppression of vagal motor activities evokes laryngeal afferent-mediated inhibition of gastric motility

Motoi Kobashi, Tomoshige Koga, Masatoshi Mizutani, Ryuji Matsuo

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

We previously reported that the activation of water-responsive afferents in the superior laryngeal nerve was responsible for the inhibition of gastric motility. The present study was undertaken to clarify the roles of the vagal preganglionic neurons responsible for laryngeal afferent-mediated inhibition of gastric motility. Intravenous injection of atropine abolished the inhibition of motility in both the distal and the proximal stomach induced by water administration into the larynx. The neurons in the dorsal motor nucleus of the vagus (DMV), which project to the abdominal viscera, were exclusively inhibited by water administration. Taken together, inhibition of neurons in the DMV induces inhibition of gastric motility evoked by laryngeal water-responsive afferents via a cholinergic pathway. Because chemical lesions of the intermediate DMV, but not the caudal DMV, abolished the inhibition of the distal stomach motility induced by water administration, the intermediate DMV is responsible for the inhibition shown in the distal stomach.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume282
Issue number3 51-3
Publication statusPublished - 2002

Fingerprint

Stomach
Motor Activity
Water
Neurons
Laryngeal Nerves
Viscera
Larynx
Inhibition (Psychology)
Atropine
Intravenous Injections
Cholinergic Agents

Keywords

  • Atropine
  • Dorsal motor nucleus of the vagus
  • Relaxation
  • Stomach
  • Superior laryngeal nerve

ASJC Scopus subject areas

  • Physiology

Cite this

Suppression of vagal motor activities evokes laryngeal afferent-mediated inhibition of gastric motility. / Kobashi, Motoi; Koga, Tomoshige; Mizutani, Masatoshi; Matsuo, Ryuji.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 282, No. 3 51-3, 2002.

Research output: Contribution to journalArticle

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