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Effects of Oxytocin on Gastric‐Projecting Neurons in a Rat Model of Functional Dyspepsia
Author(s) -
Babic Tanja,
Browning Kirsteen N,
Travagli Renato 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.701.11
Subject(s) - endocrinology , oxytocin , medicine , gabaergic , glutamate receptor , neuropeptide , chemistry , neuroscience , receptor , biology
Emotional stress triggers functional dyspepsia (FD) and gastric dysmotility. Oxytocin (OXY) modulates gastric motility and has a recognized antistressor role. We have shown that although OXY receptors are expressed in the dorsal vagal complex, OXY perfusion does not modulate the critical GABAergic inputs to identified gastric‐projecting preganglionic vagal (DMV) neurons. Here we tested the hypothesis that FD induces an abnormal response to OXY in the gastric‐related vagal circuits. Following induction of FD, we did whole‐cell patch‐clamp recordings from gastric‐projecting DMV neurons from FD and control rats. In control rats, OXY had no effect on GABA currents in any of the neurons tested unless the neurons were pretreated with the stress hormone corticotrophin releasing factor (CRF). Following CRF, OXY altered GABAcurrents in 6/15 neurons. Conversely, in FD animals, OXY altered GABA currents in 10/25 neurons, independently of CRF. In FD rats, pretreatment of neurons with H89, a protein kinase A (PKA) inhibitor, blocked the effects of OXY on GABA currents in 7/8 neurons tested. These data show that FD induces an abnormal response to OXY in the gastric‐related vagal circuits similar to that obtained by the stress‐related hormone CRF. We also suggest that that the effects are mediated by activation of cAMP/PKA pathway. Supported by: NIH DK55330