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|Title:||VPAC₁ receptors regulate intestinal secretion and muscle contractility by activating cholinergic neurons in guinea pig jejunum|
|Other Titles:||VPAC(1) receptors regulate intestinal secretion and muscle contractility by activating cholinergic neurons in guinea pig jejunum|
|Citation:||American Journal of Physiology - Gastrointestinal and Liver Physiology, 2014; 306(9):G748-G758|
|Publisher:||American Physiological Society|
|Candice Fung, Petra Unterweger, Laura J. Parry, Joel C. Bornstein and Jaime P.P. Foong|
|Abstract:||In the gastrointestinal tract, vasoactive intestinal peptide (VIP) is found exclusively within neurons. VIP regulates intestinal motility via neurally mediated and direct actions on smooth muscle and secretion by a direct mucosal action, and via actions on submucosal neurons. VIP acts via VPAC₁ and VPAC₂ receptors; however, the subtype involved in its neural actions is unclear. The neural roles of VIP and VPAC₁ receptors (VPAC₁R) were investigated in intestinal motility and secretion in guinea pig jejunum. Expression of VIP receptors across the jejunal layers was examined using RT-PCR. Submucosal and myenteric neurons expressing VIP receptor subtype VPAC₁ and/or various neurochemical markers were identified immunohistochemically. Isotonic muscle contraction was measured in longitudinal muscle-myenteric plexus preparations. Electrogenic secretion across mucosa-submucosa preparations was measured in Ussing chambers by monitoring short-circuit current. Calretinin⁺ excitatory longitudinal muscle motor neurons expressed VPAC₁R. Most cholinergic submucosal neurons, notably NPY⁺ secretomotor neurons, expressed VPAC₁R. VIP (100 nM) induced longitudinal muscle contraction that was inhibited by TTX (1 μM), PG97-269 (VPAC₁ antagonist; 1 μM), and hyoscine (10 μM), but not by hexamethonium (200 μM). VIP (50 nM)-evoked secretion was depressed by hyoscine or PG97-269 and involved a small TTX-sensitive component. PG97-269 and TTX combined did not further depress the VIP response observed in the presence of PG97-269 alone. We conclude that VIP stimulates ACh-mediated longitudinal muscle contraction via VPAC₁R on cholinergic motor neurons. VIP induces Cl(-) secretion directly via epithelial VPAC₁R and indirectly via VPAC₁R on cholinergic secretomotor neurons. No evidence was obtained for involvement of other neural VIP receptors.|
|Keywords:||Vasoactive intestinal peptide; VPAC₁ receptor; motility; secretion; enteric|
|Rights:||© 2014 the American Physiological Society|
|Appears in Collections:||Molecular and Biomedical Science publications|
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