Vagal sensory neurons are required for lipoprivic but not glucoprivic feeding in rats.
This experiment examined the role of subdiaphragmatic vagal sensory neurons in feeding stimulated by pharmacological blockade of fatty-acid oxidation (lipoprivic feeding) and glucose utilization (glucoprivic feeding). Rats prepared by surgical transection of the subdiaphragmatic vagal trunk or aspiration lesion of the vagal sensory terminal fields in the area postrema-nucleus of the solitary tract (AP-NTS) were maintained and tested on a fat-supplemented, high carbohydrate diet. Fatty-acid oxidation was blocked with mercaptoacetate (MA, 400 and 600 mumol/kg ip) and glucose utilization was blocked with 2-deoxy-D-glucose (2-DG, 100 and 200 mg/kg sc). On test days, rats were injected with MA, 2-DG, or saline, and feeding was measured hourly for 6 h beginning immediately after injection. We found that both subdiaphragmatic vagotomy and AP-NTS lesions abolished lipoprivic feeding. In contrast, glucoprivic feeding was abolished by AP-NTS lesions but not by subdiaphragmatic vagotomy. These results indicate that lipoprivic feeding requires intact subdiaphragmatic vagal sensory neurons that terminate in the AP-NTS region. Glucoprivic feeding is not vagally mediated but also requires a neural substate within the AP-NTS region.
Ritter
S
S
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman 99164-6520.
Taylor
J S
JS
D000818:Animals; D001682:Biological Availability; D002552:Cerebral Ventricles / Q000502:physiology; D003964:Diaphragm / Q000294:innervation; D004435:Eating / Q000502:physiology*; D005227:Fatty Acids / Q000494:pharmacology*; D005947:Glucose / Q000493:pharmacokinetics*; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D014628:Vagotomy / Q000379:methods; D014630:Vagus Nerve / Q000166:cytology / Q000502:physiology*
D005227:Fatty Acids; D005947:Glucose