Header

UZH-Logo

Maintenance Infos

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


Potes, C S; Riediger, T; Lutz, T A (2009). Noradrenergic neurons of the area postrema mediate amylin's anorectic action. Appetite, 52(3):853.

Abstract

Peripheral amylin inhibits food intake via activation of the area postrema (AP). 59% of amylin-activated AP neurons are noradrenergic (NA), i.e., they express dopamine-beta-hydroxylase (DBH). Here, we wanted to testwhether APNAneuronsmediate amylin’s anorectic effect.We performed a specific lesion of AP NA neurons using a saporin conjugated to an antibody against DBH (DSAP). IgG-saporin was used in sham controls. After 2–3 weeks necessary for neuronal
degeneration, we tested the rats for the effect of amylin (5
or 20_g/kg BW, s.c.) to reduce food intake. In a terminal experiment, the rats received amylin (20_g/kg) or saline; brain sections with the AP and nucleus of the solitary tract (NTS) were stained for DBH to assess lesion success and for c-Fos expression to evaluate amylin-induced neuronal activation. DBH staining revealed that 10 DSAP-injected rats had NA lesion equal to or above 50%,
defined as successful; 6 had lesions below 50%. Daily food intake and body weight gain did not differ between lesioned and sham groups. Amylin-induced anorexia was observed in sham rats with both amylin doses, while rats with a successful lesion had no significant reduction in eating after either amylin dose. Rats with lesions below 50% only ate less after the higher amylin dose. In contrast to
sham-lesioned animals, successfully NA-lesioned rats did not show amylin-induced c-Fos expression in the AP and NTS. These results provide first evidence for a functional role of NA neurons in the AP in the mediation of amylin’s anorectic effect.

Abstract

Peripheral amylin inhibits food intake via activation of the area postrema (AP). 59% of amylin-activated AP neurons are noradrenergic (NA), i.e., they express dopamine-beta-hydroxylase (DBH). Here, we wanted to testwhether APNAneuronsmediate amylin’s anorectic effect.We performed a specific lesion of AP NA neurons using a saporin conjugated to an antibody against DBH (DSAP). IgG-saporin was used in sham controls. After 2–3 weeks necessary for neuronal
degeneration, we tested the rats for the effect of amylin (5
or 20_g/kg BW, s.c.) to reduce food intake. In a terminal experiment, the rats received amylin (20_g/kg) or saline; brain sections with the AP and nucleus of the solitary tract (NTS) were stained for DBH to assess lesion success and for c-Fos expression to evaluate amylin-induced neuronal activation. DBH staining revealed that 10 DSAP-injected rats had NA lesion equal to or above 50%,
defined as successful; 6 had lesions below 50%. Daily food intake and body weight gain did not differ between lesioned and sham groups. Amylin-induced anorexia was observed in sham rats with both amylin doses, while rats with a successful lesion had no significant reduction in eating after either amylin dose. Rats with lesions below 50% only ate less after the higher amylin dose. In contrast to
sham-lesioned animals, successfully NA-lesioned rats did not show amylin-induced c-Fos expression in the AP and NTS. These results provide first evidence for a functional role of NA neurons in the AP in the mediation of amylin’s anorectic effect.

Statistics

Altmetrics

Downloads

91 downloads since deposited on 02 Nov 2009
20 downloads since 12 months
Detailed statistics

Additional indexing

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
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2009
Deposited On:02 Nov 2009 10:28
Last Modified:06 Dec 2017 20:23
Publisher:Elsevier
ISSN:0195-6663
Publisher DOI:https://doi.org/10.1016/j.appet.2009.04.158

Download

Download PDF  'Noradrenergic neurons of the area postrema mediate amylin's anorectic action'.
Preview
Filetype: PDF
Size: 1MB
View at publisher