Reflex inhibition of insulin secretion: vagus nerve involvement via CNS

The in situ brain-pancreas experimental model was used to investigate the influence of the vagus nerve during tonic direct central nervous system (CNS) inhibition of insulin secretion. Tonic CNS inhibition of insulin secretion was partially and transiently reversed following bilateral cervical vagotomy, suggesting that this inhibition includes a vagally mediated component. However, a substantial CNS inhibition of insulin secretion still occurred in the vagotomized preparations. This demonstrates that a major component producing tonic CNS inhibition of insulin secretion is independent of the vagus nerve and, furthermore, that it must be via direct sympathetic efferent pathways to the pancreas (because these preparations are functionally parasympathectomized via vagotomy). Further investigation into the vagus nerve involvement was carried out by stimulating either the afferent (central) or efferent (pancreatic) cut end of the vagus nerve of bilaterally vagotomized brain-pancreas preparations. Stimulation of the efferent vagus did not appreciably alter the effect of vagotomy on insulin secretion. However, when the central cut vagus was stimulated, the early transient reversal of tonic inhibition, which occurred in the vagotomized preparations, was totally reversed. This suggests that the vagally mediated early transient component of tonic CNS inhibition of insulin secretion is via afferent (central) neurons in the vagus nerve. These data demonstrate a reflex pathway for inhibition of insulin secretion that is comprised of vagal afferent neurons, the CNS, and sympathetic efferent neurons ending directly on the islets of Langerhans. It is tempting to speculate that gastrointestinal receptors exist that are capable of initiating this reflex inhibition of insulin secretion.