Reduced Sensory-Evoked Locus Coeruleus-Norepinephrine Neural Activity in Female Rats With a History of Dietary-Induced Binge Eating
Reduced Sensory-Evoked Locus Coeruleus-Norepinephrine Neural Activity in Female Rats With a History of Dietary-Induced Binge Eating
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DOI：
10.3389/fpsyg.2019.01966
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发表时间：
2019-09-04
影响因子：
3.8
通讯作者：
James, Morgan H.
中科院分区：
文献类型：
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作者：
Bello, Nicholas T.;Yeh, Chung-Yang;James, Morgan H.
去甲肾上腺素能通路与饮食相关的病理现象有关。这些实验旨在研究饮食诱导的暴饮暴食如何影响蓝斑（LC） - 去甲肾上腺素（NE）系统的神经元活动。年轻成年雌性斯普拉格 - 道利大鼠（7 - 8周龄）被置于一种重复间歇（每周两次）的循环中，每次有30分钟可获取一种非常可口的加糖脂肪（即含10%蔗糖的植物起酥油），同时伴有或不伴有间歇（24小时）的热量限制（分别为限制暴饮暴食组或暴饮暴食组）。年龄和体重匹配的雌性对照大鼠接受标准饲料喂养（未处理组）或间歇饲料喂养（限制组）。在2.5周后，暴饮暴食组和限制暴饮暴食组在甜脂肪食物摄入量上有所增加。在第3周，在异氟烷麻醉下记录体内单个神经元的蓝斑电生理活动。与未处理组大鼠（7只大鼠的22个细胞）相比，限制暴饮暴食组（6只大鼠的20个细胞）和暴饮暴食组（6只大鼠的27个细胞）诱发的蓝斑放电频率显著降低（分别约为20%和26%）。各组之间的自发放电频率和紧张性放电频率没有差异。在间歇接触加糖脂肪的组中，信噪比降低。为了研究饮食暴饮暴食导致的神经肽变化，在蓝斑和下丘脑弓状核（Arc）区域测量了神经肽Y（NPY）、胰高血糖素样肽1受体（GLP - 1r）、强啡肽原及相关基因的相对基因表达。在蓝斑区域，Gip - 1r、Npy2r和Pdyn随着重复间歇限制而降低。与未处理组相比，限制组弓状核中的Npyl r降低了约27%。这些数据表明，饮食诱导的暴饮暴食改变了蓝斑神经元对感觉刺激的神经反应，并抑制了神经应激反应。
Noradrenergic pathways have been implicated in eating pathologies. These experiments sought to examine how dietary-induced binge eating influences the neuronal activity of the locus coeruleus (LC)-norepinephrine (NE) system. Young adult female Sprague Dawley rats (7-8 weeks old) were exposed to a repeated intermittent (twice weekly) cycle of 30-min access to a highly palatable sweetened fat (i.e., vegetable shortening with 10% sucrose) with or without intermittent (24 h) calorie restriction (Restrict Binge or Binge groups, respectively). Age- and weight-matched female control rats were exposed to standard chow feeding (Naive group) or intermittent chow feeding (Restrict group). The Binge and Restrict Binge groups demonstrated an escalation in sweet-fat food intake after 2.5 weeks. On week 3, in vivo single-unit LC electrophysiological activity was recorded under isoflurane anesthesia. Restrict Binge (20 cells from six rats) and Binge (27 cells from six rats) had significantly reduced (approximate 20% and 26%, respectively) evoked LC discharge rates compared with naive rats (22 cells, seven rats). Spontaneous and tonic discharge rates were not different among the groups. Signal-to-noise ratio was reduced in the groups with intermittent sweetened fat exposure. In order to investigate the neuropeptide alterations as a consequence of dietary binge eating, relative gene expression of neuropeptide Y (NPY), glucagon-like peptide 1 receptor (GLP-1r), prodynorphin, and related genes were measured in LC and hypothalamic arcuate (Arc) regions. Gip-1r, Npy2r, and Pdyn in LC region were reduced with repeated intermittent restriction. Npyl r was reduced by approximately 27% in ARC of Restrict compared with Naive group. Such data indicate that dietary-induced binge eating alters the neural response of LC neurons to sensory stimuli and dampens the neural stress response.