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Göteborgs universitets publikationer

Dopamine signaling in the amygdala, increased by food ingestion and GLP-1, regulates feeding behavior.

Författare och institution:
Rozita H Anderberg (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); Christine Anefors (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); Filip Bergquist (Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi); Hans Nissbrandt (Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi); Karolina P Skibicka (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi)
Publicerad i:
Physiology & behavior, 136 s. 135–144
ISSN:
1873-507X
Publikationstyp:
Artikel, refereegranskad vetenskaplig
Publiceringsår:
2014
Språk:
engelska
Fulltextlänk:
Sammanfattning (abstract):
Mesolimbic dopamine plays a critical role in food-related reward processing and learning. The literature focuses primarily on the nucleus accumbens as the key dopaminergic target in which enhanced dopamine signaling is associated with reward. Here, we demonstrate a novel neurobiological mechanism by which dopamine transmission in the amygdala regulates food intake and reward. We show that food intake was associated with increased dopamine turnover in the amygdala. Next, we assess the impact of direct intra-amygdala D1 and D2 receptor activation on food intake and sucrose-driven progressive ratio operant conditioning in rats. Amygdala D2 receptor activation reduced food intake and operant behavior for sucrose, whereas D2 receptor blockade increased food intake but surprisingly reduced operant behavior. In contrast, D1 receptor stimulation or blockade did not alter feeding or operant conditioning for food. The glucagon-like peptide 1 (GLP-1) system, a target for type 2 diabetes treatment, in addition to regulating glucose homeostasis, also reduces food intake. We found that central GLP-1R receptor activation is associated with elevated dopamine turnover in the amygdala, and that part of the anorexic effect of GLP-1 is mediated by D2 receptor signaling in the amygdala. Our findings indicate that amygdala dopamine signaling is activated by both food intake and the anorexic brain-gut peptide GLP-1 and that amygdala D2 receptor activation is necessary and sufficient to change feeding behavior. Collectively these studies indicate a novel mechanism by which the dopamine system affects feeding-oriented behavior at the level of the amygdala.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
MEDICIN OCH HÄLSOVETENSKAP ->
Medicinska grundvetenskaper ->
Farmakologi och toxikologi ->
Farmakologi
MEDICIN OCH HÄLSOVETENSKAP ->
Medicinska grundvetenskaper ->
Neurovetenskaper ->
Neurovetenskap
Nyckelord:
Amygdala, Dopamine, Food reward, Food intake, Obesity, GLP-1, Exendin-4
Postens nummer:
203668
Posten skapad:
2014-10-03 12:20
Posten ändrad:
2016-08-19 11:27

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