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Ghrelin increases vagally mediated gastric activity by central sites of action
Author(s) -
Swartz E. M.,
Browning K. N.,
A. Travagli R.,
Holmes G. M.
Publication year - 2014
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12261
Subject(s) - ghrelin , action (physics) , medicine , endocrinology , hormone , physics , quantum mechanics
Background Vagally dependent gastric reflexes are mediated through vagal afferent fibers synapsing upon neurons of the nucleus tractus solitarius ( NTS ) which, in turn modulate the preganglionic parasympathetic dorsal motor nucleus of the vagus ( DMV ) neurons within the medullary dorsal vagal complex ( DVC ). The expression and transport of ghrelin receptors has been documented for the afferent vagus nerve, and functional studies have confirmed that vagal pathways are integral to ghrelin‐induced stimulation of gastric motility. However, the central actions of ghrelin within the DVC have not been explored fully. Methods We assessed the responses to ghrelin in fasted rats using: (i) in vivo measurements of gastric tone and motility following IVth ventricle application or unilateral microinjection of ghrelin into the DVC and (ii) whole cell recordings from gastric‐projecting neurons of the DMV . Key Results (i) IVth ventricle application or unilateral microinjection of ghrelin into the DVC ‐elicited contractions of the gastric corpus via excitation of a vagal cholinergic efferent pathway and (ii) ghrelin facilitates excitatory, but not inhibitory, presynaptic transmission to DMV neurons. Conclusions & Inferences Our data indicate that ghrelin acts centrally by activating excitatory synaptic inputs onto DMV neurons, resulting in increased cholinergic drive by way of vagal motor innervation to the stomach.