Title
Differential role of tachykinin <tex>$NK_{3}$</tex> receptors on cholinergic excitatory neurotransmission in the mouse stomach and small intestine Differential role of tachykinin <tex>$NK_{3}$</tex> receptors on cholinergic excitatory neurotransmission in the mouse stomach and small intestine
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences. Pharmacy
Faculty of Medicine and Health Sciences
Publication type
article
Publication
London ,
Subject
Pharmacology. Therapy
Human medicine
Source (journal)
British journal of pharmacology. - London
Volume/pages
155(2008) :8 , p. 1195-1203
ISSN
0007-1188
ISI
000261501300008
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
Tachykinin NK3 receptors are widely expressed in the mouse gastrointestinal tract but their functional role in enteric neuromuscular transmission remains unstudied in this species. We investigated the involvement of NK3 receptors in cholinergic neurotransmission in the mouse stomach and small intestine. Experimental approach: Muscle strips of the mouse gastric fundus and ileum were mounted in organ baths for tension recordings. Effects of NK3 agonists and antagonists were studied on contractions to EFS of enteric nerves and to carbachol. Key results: EFS induced frequency-dependent tetrodotoxin-sensitive contractions, which were abolished by atropine. The cholinergic contractions to EFS in the stomach were enhanced by the NK3 antagonist SR142801, but not affected by the NK3 agonist senktide or neurokinin B. The cholinergic contractions to EFS in the small intestine were not affected by SR142801, but dose-dependently inhibited by senktide and neurokinin B. This inhibitory effect was prevented by SR142801 but not by hexamethonium. SR142801, senktide or neurokinin B did not induce any response per se in the stomach and small intestine and did not affect contractions to carbachol. Conclusions and implications: NK3 receptors modulate cholinergic neurotransmission differently in the mouse stomach and small intestine. Blockade of NK3 receptors enhanced cholinergic transmission in the stomach but not in the intestine. Activation of NK3 receptors inhibited cholinergic transmission in the small intestine but not in the stomach. This indicates a physiological role for NK3 receptors in mouse stomach contractility and a pathophysiological role in mouse intestinal contractility.
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