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The effects of oxytocin on gastric motility are mediated by different neuronal pathways in an iodoacetamide model of functional dyspepsia
Author(s) -
Holmes Gregory M,
Travagli R. Alberto
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.701.10
Subject(s) - microinjection , endocrinology , cholinergic , medicine , vagus nerve , chemistry , oxytocin , pharmacology , stimulation
Emotional stress triggers functional dyspepsia (FD) and gastric dysmotility. Oxytocin (OXY) has a recognized antistressor role and OXY microinjection in the dorsal vagal complex induces gastric relaxation via a vagally‐mediated pathway. Our in vitro data (see abs. by Babic et al.) show that FD induces a plastic rearrangement in the gastric‐related vagal circuits so that OXY perfusion modulates the otherways unresponsive GABAergic inputs to gastric‐projecting preganglionic vagal (DMV) neurons. The aim of the present study was to investigate the in vivo mechanisms of action of OXY in a FD model. Following induction of FD, we monitored the gastric motility response induced by DMV microinjection of OXY (12.5–300pmoles). In control rats, the OXY‐mediated decrease in gastric tone peaked at a dose of 300pmoles and was antagonized by systemic administration of the NOS inhibitor, L‐NAME, which per se did not alter gastric tone. In FD rats, the dose‐response to OXY‐mediated decrease in gastric tone was shifted leftward, L‐NAME increased gastric tone and did not attenuate the OXY response. These data show that in control rats, the gastric relaxation induced by OXY is mediated by activation of a NANC vagal pathway. Following FD induction, the gastric relaxation mediated by OXY is no longer mediated by activation of a NANC pathway, but rather by inhibition of a vagal cholinergic input. Funding: NIDDK 55530