Vagal neurocircuitry and its influence on gastric motility

Abstract

A large body of research has been dedicated to the effects of gastrointestinal peptides on vagal afferent fibres, yet multiple lines of evidence indicate that gastrointestinal peptides also modulate brainstem vagal neurocircuitry, and that this modulation has a fundamental role in the physiology and pathophysiology of the upper gastrointestinal tract. In fact, brainstem vagovagal neurocircuits comprise highly plastic neurons and synapses connecting afferent vagal fibres, second order neurons of the nucleus tractus solitarius (NTS), and efferent fibres originating in the dorsal motor nucleus of the vagus (DMV). Neuronal communication between the NTS and DMV is regulated by the presence of a variety of inputs, both from within the brainstem itself as well as from higher centres, which utilize an array of neurotransmitters and neuromodulators. Because of the circumventricular nature of these brainstem areas, circulating hormones can also modulate the vagal output to the upper gastrointestinal tract. This Review summarizes the organization and function of vagovagal reflex control of the upper gastrointestinal tract, presents data on the plasticity within these neurocircuits after stress, and discusses the gastrointestinal dysfunctions observed in Parkinson disease as examples of physiological adjustment and maladaptation of these reflexes.

Intracellular emetic signaling evoked by the L-type Ca2+ channel agonist FPL64176 in the least shrew (Cryptotis parva)

“…Our lab has utilized c-Fos induction in the brainstem DVC emetic nuclei to demonstrate central responsiveness to peripheral administration of diverse emetogens (Chebolu et al, 2010; Ray et al, 2009a and 2009c; Zhong et al, 2016). In the current study participation of central emetic neurons in FPL64176-induced vomiting is further indicated by upregulated c-Fos expression in brainstem emetic nuclei NTS, a key site for integration of diverse emetic signals (Ray et al, 2009a and 2009c), and DMNX, which receives axonal projections from NTS (Travagli and Anselmi, 2016). Thus, the blood-brain barrier permeable agent FPL64176 (Jinnah et al, 1999; 2000 and 2003) could excite emetic neurons directly in the NTS and DMNX.…”

A Nigro−Vagal Pathway Controls Gastric Motility and Is Affected in a Rat Model of Parkinsonism

“…These data suggest strongly that the nigro-vagal fibers target selective subpopulations of DMV neurons dedicated to modulation of specific neurocircuits; the observation is supported also by the differential responses on tone vs motility obtained with yohimbine pretreatment. Indeed, the concept of distinct vagal neurocircuits comprising subsets of DMV neurons which modulate GI functions differentially was put forward several years ago 23 and has been supported by a wealth of evidence since 10 .…”

“…Motor commands to the upper GI tract arise from the spontaneously active, preganglionic cholinergic parasympathetic motoneurons of the DMV 8 . These neurons integrate signals from higher centers 9, 9, 10 as well as from the adjacent catecholaminergic neurons of the A2 area 11 , which provide synaptic modulation via α-adrenoceptors 12 . The efferent vagal fibers project to postganglionic myenteric neurons of the enteric nervous system (ENS) that ultimately control the motility response of the GI tract 10 .…”

Toward a Wiring Diagram Understanding of Appetite Control

“…Given this diversity of information transmitted by the sensory vagus nerve and its ~2,300 constituent neurons, a key question has been: what are the coding mechanisms used for transmitting these discrete signals? Afferents from different organs, or from different segments of the GI tract, send viscerotopic projections to subdomains of the NTS (Berthoud and Neuhuber, 2000; Travagli and Anselmi, 2016), suggesting the presence of “labeled lines” for organ-specific information. But beyond that, it has been difficult to establish coding mechanisms for different sensory modalities from within a given organ and/or specific region of the gastrointestinal (GI) tract.…”