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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-14444

Becskei, C; Grabler, V; Edwards, G L; Riediger, T; Lutz, T A (2007). Lesion of the lateral parabrachial nucleus attenuates the anorectic effect of peripheral amylin and CCK. Brain Research, 1162:76-84.

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Abstract

Amylin and CCK activate the area postrema (AP)/nucleus of the solitary tract (NTS) - lateral parabrachial nucleus (LPBN) - central amygdala (CeA) pathway. However, except for the brainstem structures the role of these nuclei for the anorectic effect of these peptides is not yet well characterized. The current study investigated the role of the LPBN in mediating the inhibitory effect of peripheral amylin and CCK on feeding behavior. Rats with electrolytic lesions in the LPBN (LPBN-X) were used in behavioral as well as in immunohistological c-Fos studies. LPBN-X significantly reduced the anorectic effect of amylin (5 microg/kg, i.p.). The effect of a higher amylin dose (10 microg/kg, i.p.) was only slightly attenuated in the LPBN-X rats. In agreement with previous studies, LPBN lesions also reduced the inhibitory effect of CCK on food intake. In the immunohistological experiments, amylin and CCK induced c-Fos expression in the AP, NTS, LPBN and CeA in the SHAM rats. Both the amylin- and CCK-induced activation of the CeA was completely abolished in the animals with a LPBN lesion. These results clearly suggest that the signal transduction pathway between the AP/NTS and CeA has been disrupted by the LPBN ablation. We conclude that the LPBN is a crucial brain site mediating the anorectic effect of amylin and CCK. Furthermore, an intact LPBN seems to be essential for the c-Fos response in the CeA induced by these peptides.

Item Type:Journal Article, refereed, original work
Communities & Collections:05 Vetsuisse Faculty > Institute of Veterinary Physiology
04 Faculty of Medicine > Center for Integrative Human Physiology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:August 2007
Deposited On:20 Mar 2009 13:55
Last Modified:27 Nov 2013 17:26
Publisher:Elsevier
ISSN:0006-8993
Publisher DOI:10.1016/j.brainres.2007.06.016
PubMed ID:17617389
Citations:Web of Science®. Times Cited: 31
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