Glucose does not activate nonadrenergic, noncholinergic inhibitory neurons in the rat stomach.
Glucose does not activate nonadrenergic, noncholinergic inhibitory neurons in the rat stomach.
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葡萄糖不会激活大鼠胃中的非肾上腺素能、非胆碱能抑制神经元。
DOI：
10.1152/ajpregu.00561.2004
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Verbalis,JosephG
中科院分区：
文献类型：
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作者：
Shi,Min;Jones,AllisonR;FerreiraJr,Manuel;Sahibzada,Niaz;Gillis,RichardA;Verbalis,JosephG
我们之前报道过，静脉注射葡萄糖作用于中枢神经系统，抑制麻醉大鼠低血糖引起的胃动力。本研究的目的是确定这种效应是否是由于迷走神经 (DMV) 胆碱能运动神经元背侧运动核的抑制（与节后胆碱能神经元突触）所致，还是由于 DMV 胆碱能神经元（与节后非肾上腺素、非胆碱能 (NANC) 神经元，特别是氮能神经元突触）的兴奋所致。 神经元。采用三种方法：1) 评估 d-葡萄糖对低血糖大鼠胃动力抑制的功效，无论是否抑制一氧化氮合酶 [10 mg/kg 静脉注射硝基-l-精氨酸甲酯 (l-NAME)]，2) 评估静脉注射氨甲酰甲胆碱 (30 μg·kg−1·min−1) 在d-葡萄糖诱导的胃运动抑制期间刺激低血糖大鼠的胃运动，3) 向正常血糖大鼠静脉注射葡萄糖后测定DMV神经元中c-Fos的表达。获得的结果表明l-NAME治疗对葡萄糖诱导的胃运动抑制没有影响；静脉注射氨甲酰甲胆碱增加胃蠕动的功效没有降低，并且投射到胃的DMV神经元中的c-Fos表达没有被d-葡萄糖诱导。这些发现表明，与节后 NANC 神经元突触的 DMV 胆碱能运动神经元的兴奋并不是 d-葡萄糖诱导的胃运动抑制的重要组成部分。
We reported previously that intravenously administeredd-glucose acts in the central nervous system to inhibit gastric motility induced by hypoglycemia in anesthetized rats. The purpose of this study was to determine whether this effect is due to inhibition of dorsal motor nucleus of the vagus (DMV) cholinergic motoneurons, which synapse with postganglionic cholinergic neurons, or to excitation of DMV cholinergic neurons, which synapse with postganglionic nonadrenergic, noncholinergic (NANC) neurons, particularly nitrergic neurons. Three approaches were employed:1) assessment of the efficacy ofd-glucose-induced inhibition of gastric motility in hypoglycemic rats with and without inhibition of nitric oxide synthase [10 mg/kg iv nitro-l-arginine methyl ester (l-NAME)],2) assessment of the efficacy of intravenous bethanechol (30 μg·kg−1·min−1) to stimulate gastric motility in hypoglycemic rats during the time ofd-glucose-induced inhibition of gastric motility, and3) determination of c-Fos expression in DMV neurons after intravenousd-glucose was administered to normoglycemic rats. Results obtained demonstrated thatl-NAME treatment had no effect ond-glucose-induced inhibition of gastric motility; there was no reduction in the efficacy of intravenous bethanechol to increase gastric motility, and c-Fos expression was not induced byd-glucose in DMV neurons that project to the stomach. These findings indicate that excitation of DMV cholinergic motoneurons that synapse with postganglionic NANC neurons is not a significant contributing component ofd-glucose-induced inhibition of gastric motility.