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Plasticity in the gastric inhibitory innervation after immunization against VIP and vagotomy in the ferret
D Grundy1, M K Gharib-Naseri, D Hutson
1Department of Biomedical Science, University of Sheffield, United Kingdom.
Changes in gastric corpus tone have been characterized during two procedures that compromise the major inhibitory innervation of the stomach: immunoneutralization of endogenous vasoactive intestinal polypeptide (VIP) and chronic vagotomy. After both procedures, there was a small but significant increase in intracorpus pressure generated during ramp increases in volume compared with sham immunized controls but not when the procedures were combined in vagotomized immunized animals. Adaptation in the mechanisms controlling corpus tone was most apparent after atropine (100 micrograms/kg) and acute vagal section when tone was low in sham immunized vagotomized and vagotomized immunized animals (4.4 +/- 0.3 and 3.7 +/- 0.8 cmH2O, respectively) and high in immunized and sham immunized animals (6.5 +/- 0.4 and 6.2 +/- 0.5 cmH2O) despite a similar sensitivity to atropine. Corpus responses to low-frequency vagal stimulation were maintained in immunized animals despite the absence of a response to exogenous VIP. We conclude that gastric reservoir function adapts to the loss of the vagal inhibitory innervation by an upregulation of intrinsic reflex pathways controlling myenteric inhibitory neurons, which are non-VIPergic.
Changes in gastric corpus tone have been characterized during two procedures that compromise the major inhibitory innervation of the stomach: immunoneutralization of endogenous vasoactive intestinal polypeptide (VIP) and chronic vagotomy. After both procedures, there was a small but significant increase in intracorpus pressure generated during ramp increases in volume compared with sham immunized controls but not when the procedures were combined in vagotomized immunized animals. Adaptation in the mechanisms controlling corpus tone was most apparent after atropine (100 micrograms/kg) and acute vagal section when tone was low in sham immunized vagotomized and vagotomized immunized animals (4.4 +/- 0.3 and 3.7 +/- 0.8 cmH2O, respectively) and high in immunized and sham immunized animals (6.5 +/- 0.4 and 6.2 +/- 0.5 cmH2O) despite a similar sensitivity to atropine. Corpus responses to low-frequency vagal stimulation were maintained in immunized animals despite the absence of a response to exogenous VIP. We conclude that gastric reservoir function adapts to the loss of the vagal inhibitory innervation by an upregulation of intrinsic reflex pathways controlling myenteric inhibitory neurons, which are non-VIPergic.