The esophageal distension-gastric relaxation response or """"""""receptive relaxation reflex"""""""" [RRR] is an autonomic mechanism which normally increases gastric volume and reduces intragastric pressure to assure that swallowed food is efficiently transported to and retained by the stomach. There is a large body of descriptive literature which supports the existence of the RRR in a number of species including rats and humans. This reflex is mediated largely, is not exclusively by a vagal afferent-CNS-vagal efferent pathway. Failure of this reflex mechanism has been held responsible for a number of serious swallowing and reflux disorders. This circuitry, which produces gastric relaxation, may also play a critical role in the perception of nausea and the production of emesis. Our preliminary results suggest that the central RR circuitry of esophageal vagal afferent connections with the nucleus of the solitary tract, pars centralis (NSTc] which, in turn, projects throughout the entire dorsal motor nucleus of the vagus [DMN]. DMN efferents which control the motility and compliance functions of the stomach are separable into two distinct vagal pathway. The other DMN projection to the stomach probably activates a non-adrenergic non-cholinergic [NANC] enteric circuit. Based on our preliminary physiological data we formulate the following hypotheses: the NSTc neurons activated by esophageal afferent input operate on these two separate DMN pathways to the stomach such that the muscarinic [""""""""excitatory""""""""] pathway is inhibited while the NANC [""""""""inhibitory""""""""] pathway is activated. The combination of effects produces a profound relaxation. Furthermore, we predict that a previously identified corticotrophin releasing hormone [CRH]- ergic CNS mechanism activated by psychological stress produces gastric stasis by activating RR circuit elements in the dorsal vagal complex. These predictions will be tested by a combination of in vivo and in vitro neurophysiological and immunocytochemical protocols.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
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General Medicine A Subcommittee 2 (GMA)
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May, Michael K
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Ohio State University
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Vance, Katie M; Rogers, Richard C; Hermann, Gerlinda E (2015) NMDA receptors control vagal afferent excitability in the nucleus of the solitary tract. Brain Res 1595:84-91
Hermann, Gerlinda E; Viard, Edouard; Rogers, Richard C (2014) Hindbrain glucoprivation effects on gastric vagal reflex circuits and gastric motility in the rat are suppressed by the astrocyte inhibitor fluorocitrate. J Neurosci 34:10488-96
Lukewich, Mark K; Rogers, Richard C; Lomax, Alan E (2014) Divergent neuroendocrine responses to localized and systemic inflammation. Semin Immunol 26:402-8
McDougal, David H; Viard, Edouard; Hermann, Gerlinda E et al. (2013) Astrocytes in the hindbrain detect glucoprivation and regulate gastric motility. Auton Neurosci 175:61-9
Viard, Edouard; Rogers, Richard C; Hermann, Gerlinda E (2012) Systemic cholecystokinin amplifies vago-vagal reflex responses recorded in vagal motor neurones. J Physiol 590:631-46
Rogers, Richard C; Hermann, Gerlinda E (2012) Tumor necrosis factor activation of vagal afferent terminal calcium is blocked by cannabinoids. J Neurosci 32:5237-41
McDougal, David H; Hermann, Gerlinda E; Rogers, Richard C (2011) Vagal afferent stimulation activates astrocytes in the nucleus of the solitary tract via AMPA receptors: evidence of an atypical neural-glial interaction in the brainstem. J Neurosci 31:14037-45
Rogers, Richard C; McDougal, David H; Hermann, Gerlinda E (2011) Leptin amplifies the action of thyrotropin-releasing hormone in the solitary nucleus: an in vitro calcium imaging study. Brain Res 1385:47-55
Barnes, Maria J; Rogers, Richard C; Van Meter, Montina J et al. (2010) Co-localization of TRHR1 and LepRb receptors on neurons in the hindbrain of the rat. Brain Res 1355:70-85
Hermann, Gerlinda E; Van Meter, Montina J; Rood, Jennifer C et al. (2009) Proteinase-activated receptors in the nucleus of the solitary tract: evidence for glial-neural interactions in autonomic control of the stomach. J Neurosci 29:9292-300

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