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Vol. 293, Issue 1, 214-221, April 2000
Department of Pharmacology and Center of Excellence for
Neuroscience, Louisiana State University Health Science Center, New
Orleans, Louisiana
Many gastrointestinal stimuli result in gastric fundic
relaxation. This information is integrated at the interface of vagal afferents and efferents in the dorsal vagal complex. Substance P (SP)
is present in this region, and the neurokinin1 receptor (NK1R) is highly expressed in preganglionic neurons of the
dorsal motor nucleus of the vagus (DMN). However, its functional
effects on vagal motor output to the stomach have not been
investigated. Therefore, we determined the gastric motor effects of
stereotaxic microinjection of SP and selective tachykinin receptor
agents into the DMN of anesthetized rats. Dose-related decreases in
intragastric pressure and antral motility were obtained on the
microinjection of SP (135 and 405 pmol) into the DMN, without
cardiovascular changes. Similar decreases in intragastric pressure were
noted after the microinjection of
[Sar9,Met(O2)11]SP
(NK1R agonist; 135 pmol) but not senktide (NK3R
agonist; 135 pmol) or vehicle. The gastric motor inhibition evoked by
SP (135 pmol) was attenuated by prior microinjection of
2-methoxy-5-tetrazol-1-yl-benzyl-(2-phenyl-piperidin-3-yl)-amine (GR203040; 1 nmol; NK1R antagonist). Vagotomy or
hexamethonium (15 mg/kg i.v.) completely abolished the gastric
relaxation evoked by SP (135 pmol) microinjected into the DMN. We
conclude that SP acts on NK1R preganglionic cholinergic
vagal neurons in the DMN, which control enteric nonadrenergic
noncholinergic motor inhibition of the fundus. The potential relevance
is that an antiemetic site of action of NK1R antagonists
may be in the DMN to prevent excitation of neurons controlling fundic
relaxation, which is an essential prodromal component of emesis.
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