Noradrenergic neurons of the area postrema mediate amylin's hypophagic action

• DOI: 10.1152/ajpregu.00791.2009
• Publication Date: 2010-06-17T02:33:29Z
• Authors: Catarina S. Potes; Victoria F. Turek; Rebecca L. Cole; Calvin Vu; Barbara L. Roland; Jonathan D. Roth; Thomas Riediger; Thomas A. Lutz
• Keywords: Area postrema; Amylin

Circulating amylin inhibits food intake via activation of the area postrema (AP). The aim this study was to identify neurochemical phenotype neurons mediating amylin's hypophagic action by immunohistochemical and feeding studies in rats. Expression c-Fos protein used as a marker for neuronal dopamine-β-hydroxylase (DBH), enzyme-catalyzing noradrenaline synthesis, noradrenergic neurons. We found that ∼50% amylin-activated AP are noradrenergic. To clarify functional role these effect on eating, noradrenaline-containing were lesioned using saporin conjugated an antibody against DBH. Amylin (5 or 20 μg/kg sc)-induced anorexia observed sham-lesioned rats with both doses. Rats lesion > 50% unresponsive low dose μg/kg) only displayed reduction 60 min after injection high (20 μg/kg). In terminal experiment, same received saline. nucleus solitary tract (NTS) stained DBH assess success expression evaluate amylin-induced activation. contrast animals, noradrenaline-lesioned did not show significant increase NTS. conclude mediate at least part effect.