Hypothalamic paraventricular nucleus lesions do not abolish glucoprivic or lipoprivic feeding.
This experiment assessed the importance of the hypothalamic paraventricular nucleus (PVN) for feeding stimulated by blockade of glucose utilization (glucoprivic feeding) and fatty acid oxidation (lipoprivic feeding). The PVN was investigated because it is innervated by neurons residing in the area postrema and nucleus of the solitary tract (AP/NTS) region where lesions have been shown to abolish both glucoprivic and lipoprivic feeding, and because the PVN appears to be a site of action for certain feeding-stimulatory peptides and amines. Bilateral electrolytic lesions were placed in the PVN and adjacent areas. Lesioned rats were subsequently tested for feeding in response to 2-deoxy-D-glucose (2DG)-and mercaptoacetate (MA)-induced blockade of glucose and fatty acid oxidation, respectively. Results revealed that total destruction of the PVN does not impair either 2DG- or MA-induced food intake and suggest that this structure is not essential for these particular controls of feeding.
Calingasan
N Y
NY
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, College of Veterinary Medicine, Washington State University, Pullman 99164-6520.
Ritter
S
S
D000818:Animals; D003847:Deoxyglucose / Q000494:pharmacology; D004032:Diet; D004435:Eating / Q000187:drug effects / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D008297:Male; D010084:Oxidation-Reduction; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013864:Thioglycolates / Q000494:pharmacology
D005227:Fatty Acids; D013864:Thioglycolates; C017487:2-mercaptoacetate; D003847:Deoxyglucose; D005947:Glucose