RESUMO
OBJECTIVE: This study replicated a model of stress-induced binge-eating in rats with a history of caloric restriction (HCR), tested their response to SSRI (fluoxetine) treatment, and explored changes in brain monoamine levels. METHOD: Young female rats with no-HCR/no-Stress, no-HCR/Stress, HCR/no-Stress, and HCR+Stress (binge-eating) were treated with fluoxetine. Post-mortem levels of serotonin, dopamine, and metabolites were assessed from brain regions key to feeding and reward. RESULTS: A 3 mg/kg dose of fluoxetine without effect in the no-HCR groups suppressed intake of HCR groups, normalizing the binge-eating of HCR/Stress rats. No differences in monoamines were detected in the hypothalamus or tegmentum but a strong positive relationship between accumbens serotonin and dopamine turnover in no-HCR rats was absent in rats with HCR. CONCLUSION: Despite lack of hunger, a history of human-like dieting alters serotonin function in ways suggesting consequences not only to feeding but also control of reward and mood that are dependent on dopamine/serotonin interactions.
Assuntos
Encéfalo/patologia , Bulimia/patologia , Dieta Redutora/efeitos adversos , Modelos Animais de Doenças , Dopamina/metabolismo , Comportamento Alimentar/fisiologia , Serotonina/metabolismo , Ácido 3,4-Di-Hidroxifenilacético/metabolismo , Animais , Antidepressivos de Segunda Geração/farmacologia , Ingestão de Energia/fisiologia , Feminino , Fluoxetina/farmacologia , Humanos , Ácido Hidroxi-Indolacético/metabolismo , Hipotálamo/patologia , Injeções Intraperitoneais , Norepinefrina/metabolismo , Núcleo Accumbens/patologia , Ratos , Ratos Sprague-Dawley , Tegmento Mesencefálico/patologiaRESUMO
The authors developed an animal model of binge eating where history of caloric restriction with footshock stress (R + S) causes rats to consume twice the normal amount of palatable food. The authors tested the hypothesis that binge eating is mediated by changes in opioid control of feeding by comparing rats' anorectic and orexigenic responses to naloxone and butorphanol, respectively, and by testing the ability of butorphanol to elicit binge eating of chow when palatable food was absent. Mu/kappa opioid-receptor blockade and activation had exaggerated responses in the R + S rats with naloxone suppressing binge eating to control levels, and although butorphanol did not trigger chow binge eating, it enhanced binge eating of palatable food. These responses in sated normal-weight rats strengthen evidence that reward, over metabolic need, drives binge eating.
