Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-43764
Potes, C S; Turek, V F; Cole, R L; Vu, C; Roland, B L; Roth, J D; Riediger, T; Lutz, T A (2010). Noradrenergic neurons of the area postrema mediate amylin's hypophagic action. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 299(2):R623-R631.
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Circulating amylin inhibits food intake via activation of the area postrema (AP). The aim of this study was to identify the neurochemical phenotype of the neurons mediating amylin's hypophagic action by immunohistochemical and feeding studies in rats. Expression of c-Fos protein was used as a marker for neuronal activation and dopamine-beta-hydroxylase (DBH), the enzyme-catalyzing noradrenaline synthesis, as a marker for noradrenergic neurons. We found that approximately 50% of amylin-activated AP neurons are noradrenergic. To clarify the functional role of these neurons in amylin's effect on eating, noradrenaline-containing neurons in the AP were lesioned using a saporin conjugated to an antibody against DBH. Amylin (5 or 20 microg/kg s.c.)-induced anorexia was observed in sham-lesioned rats with both amylin doses. Rats with a lesion of > 50% of the noradrenaline neurons were unresponsive to the low dose of amylin (5 microg/kg) and only displayed a reduction in food intake 60 min after injection of the high amylin dose (20 microg/kg). In a terminal experiment, the same rats received amylin (20 microg/kg) or saline. The AP and nucleus of the solitary tract (NTS) were stained for DBH to assess noradrenaline lesion success and for c-Fos expression to evaluate amylin-induced neuronal activation. In contrast to sham-lesioned animals, noradrenaline-lesioned rats did not show a significant increase in amylin-induced c-Fos expression in the AP and NTS. We conclude that the noradrenergic neurons in the AP mediate at least part of amylin's hypophagic effect.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Center for Integrative Human Physiology|
05 Vetsuisse Faculty > Institute of Veterinary Physiology
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||27 Jan 2011 16:02|
|Last Modified:||27 Nov 2013 22:04|
|Publisher:||American Physiological Society|
|Citations:||Web of Science®. Times Cited: 22|
Scopus®. Citation Count: 24
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