Glucose as a Regulator of Neuronal Activity

Abstract

This chapter presents glucose as a regulator of neuronal activity. Any attempt to discuss glucose exclusively as a regulator or mediator of neuronal activity would be limited, and the result superficial. It is true that glucose directly affects neurons in several peripheral organs and central neuron systems. However, these effects are modified by a host of additional nutrients, metabolites, hormones, and other peptides. In addition, glucose affects neurons that in turn affect release of these other factors, thereby, creating feedback loops having positive or negative characteristics, or that change from one to the other in different circumstances. The effects of glucose on hepatic vagal afferents have been traced, with some gaps, as far as the lateral hypothalamic (LHA) where inhibition was observed on units that were themselves identified as being directly glucose sensitive. Stimulation of the ventromedial hypothalamic (VMH), paraventricular nucleus (PVN), or splanchnic nerve decreases insulin secretion, as does LHA lesion. Conversely, LHA or vagal stimulation increases insulin secretion, and lesion of the VMH or PVN has the same effect. Glucose-responsive cells residing in the higher region of the brainstem, in the LHA and VMH, might obtain systemic glucose information from the blood or from the third ventricle.