Alpha 2 noradrenoceptors in the anterior piriform cortex decline with acute amino acid deficiency.
The responses of the brain to the amino acid deficiency that occur after eating imbalanced amino acid diets (IMB) have been associated with decreased concentrations of norepinephrine (NE) and cAMP in the anterior piriform cortex (APC), an area essential for the initial feeding responses to amino acid deficiency. In addition, the anorectic responses to IMB were decreased after injections of the alpha 2 agonist, clonidine, and increased after injections of the alpha 2 antagonist, idazoxan, into the APC. Therefore, to study the role of the alpha 2-noradrenergic receptor further in this model, we measured alpha 2-noradrenergic receptor binding in the APC of rats fed two levels of threonine IMB or a low-protein basal control diet. After basal prefeeding for 10 days, rats were given either a mild IMB, a severe IMB, or the basal diet for 2.5 h. The APC, anterior cingulate cortex (AC), ventromedial hypothalamus (VMH), and lateral hypothalamus (LH) were assayed. Binding of [3H]p-aminoclonidine to alpha 2 receptors determined that alpha 2 binding was decreased the most in APC (P < 0.0003). Binding in APC was significantly correlated with food intake in the anorectic response to IMB (P < 0.001). In AC, binding was also significantly decreased, but less dramatically (P = 0.012), and was not correlated with food intake. There were no significant changes in LH or VMH, although alpha 2-noradrenergic binding in VMH tended to decrease with the severe IMB in a pattern similar to APC. Plasma glucose values did not differ after the same feeding protocol. These data support our hypothesis that NE activity in the APC plays a role in initiating the anorectic response to IMB, perhaps via the alpha 2-noradrenergic receptor.
Gietzen
D W
DW
Department of Veterinary Anatomy, Physiology & Cell Biology and Food Intake Laboratory, University of California Davis 95616, USA.
Jhanwar-Uniyal
M
M
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000596:Amino Acids / Q000172:deficiency*; D000818:Animals; D000855:Anorexia; D001921:Brain / Q000378:metabolism*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D003000:Clonidine / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D004146:Dioxanes / Q000494:pharmacology*; D005247:Feeding Behavior; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D019329:Idazoxan; D007093:Imidazoles / Q000494:pharmacology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D009928:Organ Specificity; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000096:biosynthesis* / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000596:Amino Acids; D004146:Dioxanes; D007093:Imidazoles; D018341:Receptors, Adrenergic, alpha-2; C016986:apraclonidine; D000242:Cyclic AMP; D003000:Clonidine; D009638:Norepinephrine; D019329:Idazoxan