ABSTRACT
This chapter focuses narrowly on the cooperative participation of vagal sensory neurons and central nervous system receptors in two specific metabolic controls, the glucoprivic and lipoprivic controls, which stimulate feeding in response to decreased intracellular utilization of glucose or fatty acids, respectively. Capsaicin damages small diameter unmyelinated primary sensory neurons of both vagal and nonvagal origin as well as neurons within the brain and retina. Like the selective impairment of lipoprivic feeding by capsaicin, the selective effects of subdiaphragmatic vagotomy illustrate that the neural substrates for glucoprivic and lipoprivic feeding are different: vagal sensory neurons are necessary for lipoprivic but not for glucoprivic feeding. Lipoprivic feeding appears to be mediated by capsaicin-sensitive abdominal vagal sensory neurons that travel in more than one vagal branch. Unlike lipoprivic feeding, glucoprivic feeding does not require vagal sensory neurons, is not capsaicin sensitive and can be stimulated by independent activation of metabolic receptors within the brain.
