Dorsomedial hindbrain participation in glucoprivic feeding response to 2DG but not 2DG-induced hyperglycemia or activation of the HPA axis.
Dorsomedial hindbrain participation in glucoprivic feeding response to 2DG but not 2DG-induced hyperglycemia or activation of the HPA axis.
复制标题
背内侧后脑参与对 2DG 的糖缺乏喂养反应，但不参与 2DG 诱导的高血糖或 HPA 轴的激活。
DOI：
10.1016/s0006-8993(98)00528-9
复制
发表时间：
1998
期刊：
影响因子：
2.9
通讯作者：
Edwards,GL
中科院分区：
文献类型：
--
作者：
Edmonds,BK;Edwards,GL
2-脱氧-d-葡萄糖 (2DG) 是一种葡萄糖类似物，可抑制细胞内葡萄糖的利用，并产生一种称为糖禁喂养的特征性行为反应。后区 (AP) 是尾侧后脑结构，之前显示参与 2DG 诱导的糖缺乏喂养。此外，已知 2DG 的外周给药可引起下丘脑-垂体-肾上腺 (HPA) 轴和交感肾上腺髓质系统的激活。这些神经内分泌和对 2DG 的神经反应的神经底物尚不清楚，尽管它们也可能涉及 AP。在病变集中于后区 (APX) 的 Sprague-Dawley 大鼠和给予 2DG (200 mg/kg) 或生理盐水 (1 ml/kg) 的假手术 (SHM) 大鼠中，研究了 AP 在 2DG 诱导的进食、HPA 轴激活和高血糖中的可能作用。外周给予 2DG 会在 SHM 大鼠中引起进食反应，但在 APX 动物中则被消除。有趣的是，在药物治疗后长达 4 小时内，以该剂量施用的 2DG 使 SHM 和 APX 大鼠的血浆皮质酮和血浆葡萄糖显着增加。总的来说，这些发现表明 AP 参与外周给予 2DG 的行为（进食）反应，但似乎不是对该药物的神经内分泌（HPA 轴）和交感肾上腺（高血糖）反应的常见神经底物。
2-Deoxy-d-glucose (2DG) is a glucose analogue that inhibits intracellular utilization of glucose and produces a characteristic behavioral response known as glucoprivic feeding. The area postrema (AP) is a caudal hindbrain structure shown previously to be involved in 2DG-induced glucoprivic feeding. In addition, peripheral administration of 2DG is known to elicit activation of both the hypothalamic-pituitary-adrenal (HPA) axis and the sympathoadrenomedullary system. The neural substrates for these neuroendocrine and neural responses to 2DG are not known although they may also involve the AP. The possible role of the AP in 2DG-induced feeding, activation of the HPA axis and hyperglycemia was investigated in Sprague–Dawley rats with lesions centered on the area postrema (APX) and sham-operated (SHM) rats administered 2DG (200 mg/kg) or physiological saline (1 ml/kg). Peripheral administration of 2DG evoked a feeding response in SHM rats that was abolished in APX animals. Interestingly, 2DG administered at this dose produced a significant increase in plasma corticosterone and plasma glucose in both SHM and APX rats for up to 4 h after drug treatment. Collectively, these findings suggest that the AP is involved in the behavioral (feeding) response to peripheral administration of 2DG, but does not appear to be a common neural substrate for the neuroendocrine (HPA axis) and sympathoadrenal (hyperglycemic) responses to this agent.