TY - JOUR
T1 - Dopamine signaling in the amygdala, increased by food ingestion and GLP-1, regulates feeding behavior
AU - Anderberg, Rozita H.
AU - Anefors, Christine
AU - Bergquist, Filip
AU - Nissbrandt, Hans
AU - Skibicka, Karolina P.
N1 - Funding Information:
This manuscript is based on work presented during the 2013 Annual Meeting of the Society for the Study of Ingestive Behavior, July 30–August 3, 2013. The Swedish Research Council for Medicine ( 2011-3054 to KPS, and 2009-2618 to FB), Novo Nordisk Fonden Excellence Award (KPS), Sahlgrenska Faculty Fund (KPS), and Harald Jeanssons Stiftelse and Greta Jeanssons Stiftelse (KPS) funded the study.
Publisher Copyright:
© 2014 Elsevier Inc.
PY - 2014/9/1
Y1 - 2014/9/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84917732297&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84917732297&partnerID=8YFLogxK
U2 - 10.1016/j.physbeh.2014.02.026
DO - 10.1016/j.physbeh.2014.02.026
M3 - Article
AN - SCOPUS:84917732297
VL - 136
SP - 135
EP - 144
JO - Physiology and Behavior
JF - Physiology and Behavior
SN - 0031-9384
ER -