Central Cholinergic Descending Pathway to the Dorsal Motor Nucleus of the Vagus in Regulation of Gastric Functions

A possible role of the cholinergic mechanism within the dorsal motor nucleus of the vagus (NDV) in the regulation of gastric functions was examined in urethane anesthetized rats. Pretreatment with atropine (1–5 nmole). intracerebroventricularly inhibited the increase in both gastric acid output and...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1986, Vol.41(3), pp.373-379
Main Authors: OKUMA, Yasunobu, OSUMI, Yoshitsugu
Format: Article
Language:English
Subjects:
Animals
Atropine - pharmacology
Brain Mapping
Cholinergic Fibers - physiology
Efferent Pathways - physiology
Gastric Acid - metabolism
Gastric Mucosa - blood supply
Hypothalamic Area, Lateral - physiology
Male
Medulla Oblongata - physiology
Rats
Rats, Inbred Strains
Stomach - innervation
Vagus Nerve - physiology
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Summary:A possible role of the cholinergic mechanism within the dorsal motor nucleus of the vagus (NDV) in the regulation of gastric functions was examined in urethane anesthetized rats. Pretreatment with atropine (1–5 nmole). intracerebroventricularly inhibited the increase in both gastric acid output and mucosal blood flow (MBF). as induced by electrical stimulation of the lateral hypothalamic area (LHA). Bethanechol. micromjected into the dorsal vagal complex (the NDV. the nucleus tractus solitanus and area postrema) induced dose-dependent (5–30 nmole) increases in gastric acid output and MBF, while nicotine was without effect Pretreatment with atropine 3 nmole microinjected into the dorsal vagal complex completely blocked the increases induced by electrical stimulation of the LHA Furthermore, the increases in these gastric parameters induced by the administration of 2-deoxy-D-glucose (2-DG) were also significantly inhibited by atropine micromjected into the dorsal vagal complex. These results suggest that neurotransmission of the central descending pathway to the NDV in excitatory regulation of gastric functions is probably mediated through cholinergic muscarinic receptors.
ISSN:0021-5198
1347-3506
DOI:10.1254/jjp.41.373