کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2012967 1541859 2014 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Dietary-induced binge eating increases prefrontal cortex neural activation to restraint stress and increases binge food consumption following chronic guanfacine
ترجمه فارسی عنوان
خوردن غذا ناشی از رژیم غذایی باعث افزایش فعالیت عصبی قشر پیش از قاعدگی می شود تا استرس را محدود کند و مصرف غذای مصرفی را بعد از گینافاسین مزمن افزایش دهد
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
چکیده انگلیسی


• Dietary conditions can promote binge-like eating and alter stress responses.
• Increased c-Fos in the dorsal mPFC to sweet fat food was found in bingeing rats.
• Neural activation was elevated following acute restraint stress.
• Chronic delivery of an alpha 2A adrenergic agonist increased binge-like eating.

Binge eating is a prominent feature of bulimia nervosa and binge eating disorder. Stress or perceived stress is an often-cited reason for binge eating. One notion is that the neural pathways that overlap with stress reactivity and feeding behavior are altered by recurrent binge eating. Using young adult female rats in a dietary-induced binge eating model (30 min access to binge food with or without 24-h calorie restriction, twice a week, for 6 weeks) we measured the neural activation by c-Fos immunoreactivity to the binge food (vegetable shortening mixed with 10% sucrose) in bingeing and non-bingeing animals under acute stress (immobilization; 1 h) or no stress conditions. There was an increase in the number of immunopositive cells in the dorsal medial prefrontal cortex (mPFC) in stressed animals previously exposed to the binge eating feeding schedules. Because attention deficit hyperactive disorder (ADHD) medications target the mPFC and have some efficacy at reducing binge eating in clinical populations, we examined whether chronic (2 weeks; via IP osmotic mini-pumps) treatment with a selective alpha-2A adrenergic agonist (0.5 mg/kg/day), guanfacine, would reduce binge-like eating. In the binge group with only scheduled access to binge food (30 min; twice a week; 8 weeks), guanfacine increased total calories consumed during the 30-min access period from the 2-week pre-treatment baseline and increased binge food consumption compared with saline-treated animals. These experiments suggest that mPFC is differentially activated in response to an immobilization stress in animals under different dietary conditions and chronic guanfacine, at the dose tested, was ineffective at reducing binge-like eating.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology Biochemistry and Behavior - Volume 125, October 2014, Pages 21–28
نویسندگان
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