Blockade by glutamic acid diethyl ester of excitation of nucleus tractus solitarii neurons and vasodepressor responses reflexly elicited by vagal stimulation.
Blockade by glutamic acid diethyl ester of excitation of nucleus tractus solitarii neurons and vasodepressor responses reflexly elicited by vagal stimulation.
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谷氨酸二乙酯阻断孤束核神经元的兴奋和由迷走神经刺激引起的反射性血管抑制反应。
DOI：
10.1016/0014-2999(83)90612-x
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发表时间：
1983
影响因子：
5
通讯作者：
Reis,DJ
中科院分区：
文献类型：
--
作者：
Granata,AR;Reis,DJ
我们调查了麻醉的（乌拉坦1.5g/kg ip），麻痹和通气大鼠，谷氨酸（1-Glu）拮抗剂谷氨酸二乙酯（GDEE）对孤束核（NTS）神经元兴奋的影响，特征为“心血管”（CV）通过它们对迷走神经刺激和去甲肾上腺素升高血压产生的压力感受器刺激的反应来改变其放电率的能力（NE）。利用细胞外记录技术，我们分析了迷走神经刺激对延髓75个细胞的影响。迷走神经刺激改变了60/75个单位的活动。在迷走神经刺激过程中，60个反应神经元中有33个增加，而27个降低了它们的放电率。在10个由迷走神经刺激兴奋的细胞中：（a）第一个记录的尖峰的潜伏期在3-6 ms之间变化（x= 4.2 ms）;（B）重复刺激呈现的潜伏期不稳定;（c）NE升高动脉压引起的压力感受器刺激增加神经元活动;（d）该组的所有细胞都位于背侧NTS。在所有10个细胞中，全身GDEE（180 mg/kg iv）可逆地阻断诱发的尖峰和反射性心动过缓和低血压引起的电刺激迷走神经。GDEE不能阻断电刺激三叉神经复合体的血管降压反应。为了证明GDEE是NTS中的1-Glu拮抗剂，发现在8个以心血管为特征的细胞中，用多管移液管用微泵释放1-Glu，增加神经元活性。在70%的这些细胞中，通过相同的方法释放的GDEE可逆地阻断了1-Glu的兴奋作用。我们的结论是，在NTS的一些神经元，迷走神经传入和压力感受器刺激驱动，被1-Glu的拮抗剂。
We investigated in anesthetized (urethane 1.5 g/kg ip), paralyzed and ventilated rats, the effect of the glutamic acid (1-Glu) antagonist, glutamic acid diethyl ester (GDEE), on the excitation of neurons in the nucleus tractus solitarii (NTS), characterized as ‘cardiovascular’(CV) by their capacity to modify their firing rate in response to vagal stimulation and to baroreceptor stimulation produced by elevating blood pressure by norepinephrine (NE). Using an extracellular recording technique, we analyzed the effect of vagus stimulation on 75 cells in the medulla. Vagal stimulation modified the activity of 60/75 units. Thirty-three of the 60 responsive neurons increased, while 27 decreased their firing rate during vagal stimulation. In 10 cells excited by vagal stimulation:(a) the latency of the first recorded spike varied between 3–6 ms (x= 4.2 ms);(b) the latency to repeated stimulus presentation was unstable;(c) neuronal activity was increased by baroreceptor stimulation elicited by elevating arterial pressure with NE;(d) all of the cells of this group were located in the dorsal NTS. In all 10 cells, systemic GDEE (180 mg/kg iv) reversibly blocked both the evoked spikes and the reflex bradycardia and hypotension induced by electrical stimulation of the vagus. GDEE failed to block the vasodepressor response to electrical stimulation of the trigeminal complex. To demonstrate that GDEE is an 1-Glu antagonist in the NTS, it was found that in 8 cells characterized as cardiovascular, 1-Glu released with a micropump from a multibarrel pipette, increased the neuronal activity. In 70% of these cells, GDEE released by the same method reversibly blocked the excitatory effect of 1-Glu. We conclude that some neurons in the NTS, driven by vagal afferents and baroreceptor stimulation, are blocked by an antagonist of 1-Glu.