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Plasticity of vagal neurocircuits that control gastrointestinal motility in normal and pathophysiological conditions

      Stress is pivotal to the development and/or exacerbation of functional gastrointestinal (GI) disorders. An emerging body of evidence suggests that the gut-brain axis influences neuroplasticity and adaptation to stress through vagal sensory-motor functions. The brainstem vagal neurocircuitry comprises afferent vagal fibers impinging onto neurons of the nucleus tractus solitarius (NTS), whose neurons project to, among other areas, the adjacent preganglionic neurons of the dorsal motor nucleus of the vagus (DMV). This neurocircuitry integrates metabolic and hormonal signals with inputs from other higher CNS centers, including projections from the paraventricular nucleus of the hypothalamus (PVN). Increasing active and passive tactile stimulation to both infants and rodents improves maturation and development of visceral neurocircuitry, including vago-hypothalamic viscero-sensory projections, suggesting that interventions that rewire central neurocircuitry may have positive outcomes on vagally-mediated GI functions and possibly reverse stress-induced GI dysfunctions. Parvocellular PVN neurons are the sole source of the prototypical anti-stress hormone oxytocin (OXY) to brainstem vagal neurons. These neurons are activated by stressful stimuli, as well as food intake and social attachment, and receive reciprocal influences from brainstem vagal neurons, especially A2 catecholaminergic neurons. Further, acute restraint stress delays gastric emptying and accelerates colonic transit; this stress-induced GI dysmotility is absent after chronic homotypic stress. This adaptation may involve an OXY-dependent mechanism, since the restored motility is reversed by OXY deficiency or by icv injection of an OXY antagonist. In this presentation, we will discuss experimental approaches aimed at assessing the role of OXY in stress-related GI functions.
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