Estradiol treatment increases feeding-induced c-Fos expression in the brains of ovariectomized rats
Estradiol treatment increases feeding-induced c-Fos expression in the brains of ovariectomized rats
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DOI：
10.1152/ajpregu.2001.281.3.r738
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发表时间：
2001-09-01
影响因子：
2.8
通讯作者：
Geary, N
中科院分区：
文献类型：
--
作者：
Eckel, LA;Geary, N
类固醇激素雌二醇通过增加与进餐终止相关的负反馈信号的效力来减少进餐量。我们使用 c-Fos 免疫组织化学（神经元激活标记物）来研究雌二醇调节孤束核 (NTS) 内进食诱导的负反馈信号处理的假设，孤束核是控制食物摄入的神经元网络的第一个中枢中继站，以及与食物摄入控制相关的其他大脑区域。连续2天给喂食、切除卵巢的大鼠皮下注射10杯17-β雌二醇苯甲酸酯或芝麻油载体。第二次注射后 48 小时，在天黑开始时给予 0、5 或 10 毫升熟悉的甜牛奶饮食 20 分钟。 100 分钟后对大鼠进行灌注，收集脑组织并进行处理以检测 c-Fos 样免疫反应性。在油处理的大鼠中，喂食增加了 NTS、下丘脑室旁核 (PVN) 和杏仁核中央核 (CeA) 中 c-Fos 阳性细胞的数量。雌二醇治疗进一步增强了尾部、后部和中间 NTS 的这种反应，这些 NTS 处理负反馈饱足感信号，但在头侧 NTS 中则没有这种反应，而头侧 NTS 处理控制膳食大小的正反馈味觉信号。雌二醇治疗还增加了 PVN 和 CeA 中喂养诱导的 c-Fos。这些结果表明，适量的食物会增加去卵巢大鼠大脑区域内与控制膳食量有关的神经元活动，并且雌二醇治疗选择性地增加这种激活。他们还表明，雌二醇通过增加控制膳食量的分布式神经网络多个区域中与进食相关的神经元活动来减少膳食量。
The steroid hormone estradiol decreases meal size by increasing the potency of negative-feedback signals involved in meal termination. We used c-Fos immunohistochemistry, a marker of neuronal activation, to investigate the hypothesis that estradiol modulates the processing of feeding-induced negative-feedback signals within the nucleus of the solitary tract (NTS), the first central relay of the neuronal network controlling food intake, and within other brain regions related to the control of food intake. Chow-fed, ovariectomized rats were injected subcutaneously with 10 mug 17-beta estradiol benzoate or sesame oil vehicle on 2 consecutive days. Forty-eight hours after the second injections, 0, 5, or 10 ml of a familiar sweet milk diet were presented for 20 min at dark onset. Rats were perfused 100 min later, and brain tissue was collected and processed for c-Fos-like immunoreactivity. Feeding increased the number of c-Fos-positive cells in the NTS, the paraventricular nucleus of the hypothalamus (PVN), and the central nucleus of the amygdala (CeA) in oil-treated rats. Estradiol treatment further increased this response in the caudal, subpostremal, and intermediate NTS, which process negative-feedback satiation signals, but not in the rostral NTS, which processes positive-feedback gustatory signals controlling meal size. Estradiol treatment also increased feeding-induced c-Fos in the PVN and CeA. These results indicate that modest amounts of food increase neuronal activity within brain regions implicated in the control of meal size in ovariectomized rats and that estradiol treatment selectively increases this activation. They also suggest that estradiol decreases meal size by increasing feeding-related neuronal activity in multiple regions of the distributed neural network controlling meal size.