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前边缘皮层深部脑刺激可减少慢性暴饮暴食大鼠模型中的暴饮暴食量。

Prelimbic Cortex Deep Brain Stimulation Reduces Binge Size in a Chronic Binge Eating Rat Model.

作者信息

Sarica Can, Ozkan Mazhar, Hacioglu Bay Husniye, Sehirli Umit, Onat Filiz, Ziyal M Ibrahim

机构信息

Department of Neurosurgery, Marmara University, Istanbul, Turkey.

Institute of Neurological Sciences, Marmara University, Istanbul, Turkey.

出版信息

Stereotact Funct Neurosurg. 2018;96(1):33-39. doi: 10.1159/000486965. Epub 2018 Mar 13.

Abstract

BACKGROUND

Binge eating (BE) involves the consumption of a large amount of food in a short period of time and a loss of control during the binge episode. It is a key feature of the major subtypes of eating disorders like bulimia nervosa, BE disorder, anorexia nervosa binge/purge type. Alterations in the mesocorticolimbic pathway play a crucial role in its pathophysiology.

OBJECTIVES

We hypothesized that BE rats receiving deep brain stimulation (DBS) in the prelimbic cortex, a functional analog of the dorsolateral prefrontal cortex in humans, would have a reduced binge size compared with those receiving sham stimulation.

METHODS

Eight male Sprague-Dawley rats were implanted with a DBS electrode in the left prelimbic cortex. A protocol which included limited access to a "sweet-fat" diet was used to achieve a chronic BE state in the rats. After reaching a stable binge size, each rat had undergone sham, low-frequency stimulation (60 Hz), and high-frequency (130 Hz) stimulation for 3 sessions each, and 2 consecutive treatments were separated by at least 2 empty sessions to allow a washout of the effects. A one-way ANOVA was used for the data analysis.

RESULTS

Low-frequency (60 Hz) stimulation of the prelimbic cortex significantly reduced the binge size compared to the sham stimulation (p < 0.0001). High-frequency DBS (130 Hz) had no significant influence on this behavior when compared to sham stimulation (p = 0.9).

CONCLUSIONS

This study suggests that low-frequency prelimbic cortex stimulation in BE would be useful for correcting prefrontal hypofunction which is strongly associated with BE and addiction pathogenesis.

摘要

背景

暴饮暴食(BE)是指在短时间内摄入大量食物,且在暴饮暴食期间失去控制。它是神经性贪食症、暴饮暴食症、神经性厌食症暴食/清除型等主要饮食失调亚型的关键特征。中脑皮质边缘通路的改变在其病理生理学中起关键作用。

目的

我们假设,与接受假刺激的大鼠相比,在人类背外侧前额叶皮质的功能类似物——前边缘皮质接受深部脑刺激(DBS)的暴饮暴食大鼠的暴饮暴食量会减少。

方法

八只雄性Sprague-Dawley大鼠在左侧前边缘皮质植入DBS电极。采用一种包括限制获取“甜-脂”饮食的方案,使大鼠达到慢性暴饮暴食状态。在达到稳定的暴饮暴食量后,每只大鼠分别接受假刺激、低频刺激(60赫兹)和高频(130赫兹)刺激,各进行3次,且连续两次治疗之间至少间隔2次空刺激,以消除影响。数据分析采用单因素方差分析。

结果

与假刺激相比,前边缘皮质的低频(60赫兹)刺激显著减少了暴饮暴食量(p < 0.0001)。与假刺激相比,高频DBS(130赫兹)对这种行为没有显著影响(p = 0.9)。

结论

本研究表明,对暴饮暴食大鼠进行前边缘皮质低频刺激有助于纠正与暴饮暴食和成瘾发病机制密切相关的前额叶功能减退。

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