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1 Institute of Veterinary Physiology, Universitiy of Zurich, Zurich, Switzerland
* To whom correspondence should be addressed. E-mail: triedig{at}vetphys.unizh.ch.
Amylin is a peptide hormone which is co-secreted with insulin from the pancreas during and after food-intake. Peripherally injected amylin potently inhibits feeding by acting on the area postrema (AP), a circumventricular organ (CVO) lacking a functional blood-brain-barrier (BBB). We recently demonstrated that AP neurons are excited by a near physiological concentration of amylin. However, the subsequent neuronal mechanisms and the relevance of endogenously released amylin for the regulation of food intake are poorly understood. Therefore, we investigated 1) amylin's contribution to feeding-induced c-fos expression in the rat AP and its ascending projection sites, and 2) amylin's ability to reverse fasting-induced c-fos expression in the lateral hypothalamic area (LHA). Similar to amylin (20 µg/kg, s.c.), refeeding of 24 hr food-deprived rats induced c-fos expression in the AP, the nucleus of the solitary tract (NTS), the lateral parabrachial nuclues (LPBN) and the central nucleus of the amygdala (CeA). In AP-lesioned rats, the amylin-induced c-fos expression in each of these sites was blunted, indicating an AP-mediated activation of these structures. Pretreatment with the amylin antagonist AC187 (1 mg/kg s.c.) inhibited feeding-induced c-fos expression in the AP. Food deprivation activated LHA neurons, a response known to be associated with hunger. This effect was reversed within 2 hr after refeeding and also in non-refed animals that received amylin. In summary, our data provide first evidence that feeding-induced amylin release activates AP-neurons projecting to subsequent relay stations known to transmit meal-related signals to the forebrain. Activation of this pathway seems to coincide with an inhibition of LHA neurons.
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