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CRF-CRF1 receptor system in the central and basolateral nuclei of the amygdala differentially mediates excessive eating of palatable food.

ABSTRACT: Highly palatable foods and dieting are major contributing factors for the development of compulsive eating in obesity and eating disorders. We previously demonstrated that intermittent access to palatable food results in corticotropin-releasing factor-1 (CRF1) receptor antagonist-reversible behaviors, which include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior. However, the brain areas mediating these effects are still unknown. Male Wistar rats were either fed chow continuously for 7 days/week (Chow/Chow group), or fed chow intermittently 5 days/week, followed by a sucrose, palatable diet 2 days/week (Chow/Palatable group). Following chronic diet alternation, the effects of microinfusing the CRF1 receptor antagonist R121919 (0, 0.5, 1.5??g/side) in the central nucleus of the amygdala (CeA), the basolateral nucleus of the amygdala (BlA), or the bed nucleus of the stria terminalis (BNST) were evaluated on excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior. Furthermore, CRF immunostaining was evaluated in the brain of diet cycled rats. Intra-CeA R121919 blocked both excessive palatable food intake and anxiety-like behavior in Chow/Palatable rats, without affecting chow hypophagia. Conversely, intra-BlA R121919 reduced the chow hypophagia in Chow/Palatable rats, without affecting excessive palatable food intake or anxiety-like behavior. Intra-BNST treatment had no effect. The treatments did not modify the behavior of Chow/Chow rats. Immunohistochemistry revealed an increased number of CRF-positive cells in CeA--but not in BlA or BNST--of Chow/Palatable rats, during both withdrawal and renewed access to the palatable diet, compared with controls. These results provide functional evidence that the CRF-CRF1 receptor system in CeA and BlA has a differential role in mediating maladaptive behaviors resulting from palatable diet cycling.

SUBMITTER: Iemolo A

PROVIDER: S-EPMC3799065 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature

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CRF-CRF1 receptor system in the central and basolateral nuclei of the amygdala differentially mediates excessive eating of palatable food.

Iemolo Attilio A Blasio Angelo A St Cyr Stephen A SA Jiang Fanny F Rice Kenner C KC Sabino Valentina V Cottone Pietro P

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 20130610 12

Highly palatable foods and dieting are major contributing factors for the development of compulsive eating in obesity and eating disorders. We previously demonstrated that intermittent access to palatable food results in corticotropin-releasing factor-1 (CRF1) receptor antagonist-reversible behaviors, which include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior. However, the brain areas mediating these effects are still unknown. Male Wistar rats were eithe ...[more]

PMID: 23748225

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Project description:Stress is a complex human experience and having both rewarding and aversive motivational properties. The adverse effects of stress are well documented, yet many of underlying mechanisms remain unclear and controversial. Here we report that the anxiogenic properties of stress are encoded by the endogenous opioid peptide dynorphin acting in the basolateral amygdala. Using pharmacological and genetic approaches, we found that the anxiogenic-like effects of Corticotropin Releasing Factor (CRF) were triggered by CRF(1)-R activation of the dynorphin/kappa opioid receptor (KOR) system. Central CRF administration significantly reduced the percent open-arm time in the elevated plus maze (EPM). The reduction in open-arm time was blocked by pretreatment with the KOR antagonist norbinaltorphimine (norBNI), and was not evident in mice lacking the endogenous KOR ligand dynorphin. The CRF(1)-R agonist stressin 1 also significantly reduced open-arm time in the EPM, and this decrease was blocked by norBNI. In contrast, the selective CRF(2)-R agonist urocortin III did not affect open arm time, and mice lacking CRF(2)-R still showed an increase in anxiety-like behavior in response to CRF injection. However, CRF(2)-R knockout animals did not develop CRF conditioned place aversion, suggesting that CRF(1)-R activation may mediate anxiety and CRF(2)-R may encode aversion. Using a phosphoselective antibody (KORp) to identify sites of dynorphin action, we found that CRF increased KORp-immunoreactivity in the basolateral amygdala (BLA) of wildtype, but not in mice pretreated with the selective CRF(1)-R antagonist, antalarmin. Consistent with the concept that acute stress or CRF injection-induced anxiety was mediated by dynorphin release in the BLA, local injection of norBNI blocked the stress or CRF-induced increase in anxiety-like behavior; whereas norBNI injection in a nearby thalamic nucleus did not. The intersection of stress-induced CRF and the dynorphin/KOR system in the BLA was surprising, and these results suggest that CRF and dynorphin/KOR systems may coordinate stress-induced anxiety behaviors and aversive behaviors via different mechanisms.

Project description:Eating behavior is not only influenced by the current energy balance, but also by the behavioral characteristics of eating. One of the recognized eating behavior constructs is 'disinhibited eating,' which refers to the tendency to overeat in response to negative emotional states or the presence of highly palatable foods. Food-related disinhibition is involved in binge eating, weight gain, and obesity and is also associated with the trait of impulsivity, which in turn, is linked to weight gain or maladaptive eating. However, the relationships among food-related disinhibition, the trait of impulsivity, and the neural substrates of eating behaviors in adolescence remain unclear. Therefore, we designed a functional magnetic resonance imaging (fMRI) study to examine the associations between brain responses to palatable liquid consumption and disinhibited eating behavior or impulsivity in healthy adolescents. Thirty-four adolescents (mean age ± standard deviation = 17.12 ± 1.91 years, age range = 14-19 years, boys = 15, girls = 19) participated in this study. Disinhibited eating was assessed with the disinhibition subscale of the Three-Factor Eating Questionnaire, while impulsivity was assessed using the Barratt impulsiveness scale. Participants received two fMRI sessions-a palatable liquid consumption fMRI and a resting-state fMRI. The fMRI experiment showed that increased disinhibited eating was positively associated with a greater insular response to palatable liquid consumption, while increased impulsivity was positively correlated with a greater amygdala response. The resting-state fMRI experiment showed that increased disinhibited eating was positively correlated with strengthened intrinsic functional connectivity between the insula and the amygdala, adjusting for sex (estimates of the beta coefficients = 0.146, standard error = 0.068, p = 0.040). Given that the amygdala and insular cortex are structurally and functionally connected and involved in trait impulsivity and ingestive behavior, our findings suggest that increased disinhibited eating would be associated with impulsivity via strengthened intrinsic functional connectivity between the insula and amygdala and linked to maladaptive eating.

Dataset Information

CRF-CRF1 receptor system in the central and basolateral nuclei of the amygdala differentially mediates excessive eating of palatable food.

Publications

CRF-CRF1 receptor system in the central and basolateral nuclei of the amygdala differentially mediates excessive eating of palatable food.

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