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L-精氨酸衍生的一氧化氮合成对孤束核神经元活动的影响。

Effects of L-arginine-derived nitric oxide synthesis on neuronal activity in nucleus tractus solitarius.

作者信息

Ma S, Abboud F M, Felder R B

机构信息

Cardiovascular Center, University of Iowa College of Medicine, Iowa City 52242.

出版信息

Am J Physiol. 1995 Feb;268(2 Pt 2):R487-91. doi: 10.1152/ajpregu.1995.268.2.R487.

Abstract

The purpose of these studies was to determine the effects of L-arginine-derived nitric oxide (NO) synthesis on neuronal activity in solitary tract nucleus (NTS) neurons. Single unit activity was recorded extracellularly from medial NTS neurons in Fischer-344 rats in vivo and in vitro. In anesthetized rats with arterial pressure maintained constant, NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv), an inhibitor of NO synthesis, decreased the discharge rate in 12 of 14 neurons and increased the discharge rate in two. After injection of L-NAME, the slowing of neuronal activity began within 2-5 min, and maximal responses were observed 12-15 min after injection. The decreases in activity were reversed within 12-15 min with L-arginine (30 mg/kg iv) or immediately with nitroglycerin (NTG, 10-30 micrograms/kg iv). In superfused rat brain slices, the discharge rate was reduced by 1 mM L-NAME in seven neurons, increased in two, and unchanged in one. The decreases in discharge rate were reversed by 2 mM L-arginine (4 of 6 neurons) and by 10-30 microM NTG (6 of 7 neurons). The results show that L-arginine-derived NO can affect the spontaneous discharge rate of NTS neurons. We conclude that NO may influence the excitability of NTS neurons involved in central autonomic control.

摘要

这些研究的目的是确定L-精氨酸衍生的一氧化氮(NO)合成对孤束核(NTS)神经元神经活动的影响。在体内和体外记录Fischer-344大鼠内侧NTS神经元的单单位活动。在动脉压保持恒定的麻醉大鼠中,NO合成抑制剂NG-硝基-L-精氨酸甲酯(L-NAME,10mg/kg静脉注射)使14个神经元中的12个放电率降低,2个神经元的放电率增加。注射L-NAME后,神经活动减慢在2-5分钟内开始,注射后12-15分钟观察到最大反应。用L-精氨酸(30mg/kg静脉注射)在12-15分钟内或立即用硝酸甘油(NTG,10-30μg/kg静脉注射)可逆转活动的降低。在灌流的大鼠脑片中,1mM L-NAME使7个神经元的放电率降低,2个神经元的放电率增加,1个神经元的放电率不变。2mM L-精氨酸(6个神经元中的4个)和10-30μM NTG(7个神经元中的6个)可逆转放电率的降低。结果表明,L-精氨酸衍生的NO可影响NTS神经元的自发放电率。我们得出结论,NO可能影响参与中枢自主控制的NTS神经元的兴奋性。

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