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Chemical mediators of spinal inhibition of rat sympathetic neurones on stimulation in the nucleus tractus solitarii.

机译:脊髓抑制大鼠交感神经刺激脊髓的化学介质。

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摘要

1. This study was undertaken to gain more direct evidence of the pathways and neurochemical mediators of a spinally mediated baroreceptor inhibition of sympathetic preganglionic neurones (SPNs). 2. For this purpose, single-pulse electrical stimulation within identified vasodepressor regions of the nucleus tractus solitarii (NTS) was used together with extracellular recordings of single antidromically identified SPNs in the T2 segment of the spinal cord of anaesthetized rats. 3. The actions of agonists and antagonists of inhibitory amino acids on the NTS-induced inhibitions were determined, when they were iontophoretically applied in the vicinity of SPNs via a multibarrel micropipette assembly. 4. Extracellular recordings were made from sixty-nine SPNs. In forty-four SPNs, NTS stimulation elicited a period of inhibition of activity in both spontaneous and 'D,L-homocysteic acid-driven' SPNs with a latency to onset of 60 +/- 6 ms and a magnitude of 80 +/- 3%. 5. In six out of eight neurones, the NTS-induced inhibition was reduced by 74 +/- 16% during the application of the glycine antagonist strychnine (0-10 nA, 5-10 min) with doses that selectively blocked the inhibitory effect of iontophoretically applied glycine. 6. In nine out of nine neurones, the NTS-induced inhibition was reduced by 38 +/- 6% during the application of the GABAA antagonist bicuculline (5-15 nA, 4-14 min) with doses that selectively blocked the inhibitory effect of iontophoretically applied GABA. 7. In two SPNs, the actions of strychnine and bicuculline were shown to be additive in blocking the NTS inhibition. 8. The selective GABAB antagonists, CGP 35348 (20-50 nA, 6-25 min) and CGP 55845A (10 nA, 11 min) did not antagonize the NTS-induced inhibition. 9. It is suggested that GABA and glycine interneurones are activated by a baroreceptor bulbospinal pathway to inhibit sympathetic preganglionic neurones in the spinal cord.
机译:1.这项研究旨在获得脊髓介导的压力感受器抑制交感神经节前神经元(SPNs)的途径和神经化学介质的更直接证据。 2.为此,将单脉冲电刺激在孤核(NTS)的已确定的血管舒缩压区域内使用,并在麻醉的大鼠的脊髓T2区段中使用单抗线鉴定的SPN的细胞外记录。 3.确定了激动剂和抑制性氨基酸拮抗剂对NTS诱导的抑制作用的作用,方法是通过多管微量移液器将它们离子导入到SPN附近。 4.从69个SPN进行细胞外记录。在44个SPN中,NTS刺激在自发性和“ D,L-同型半胱氨酸驱动”的SPN中引起了一定的活性抑制期,发作潜伏期为60 +/- 6毫秒,幅度为80 +/-。 3%。 5.在八种神经元中,有六种在选择性地阻断抑制作用的剂量应用甘氨酸拮抗剂士的宁(0-10 nA,5-10分钟)的过程中,NTS诱导的抑制作用降低了74 +/- 16%。离子电渗疗法应用的甘氨酸。 6.在九种神经元中的九种中,在有选择性地阻断抑制作用的剂量的GABAA拮抗剂双小分子(5-15 nA,4-14分钟)的应用期间,NTS诱导的抑制作用降低了38 +/- 6%。离子电渗疗法应用的GABA。 7.在两个SPN中,士的宁和双瓜氨酸的作用被证明在阻止NTS抑制中具有加和作用。 8.选择性的GABA B拮抗剂CGP 35348(20-50 nA,6-25分钟)和CGP 55845A(10 nA,11分钟)没有拮抗NTS诱导的抑制作用。 9.建议GABA和甘氨酸中间神经元被压力感受器球脊髓途径激活,以抑制脊髓中的交感神经节前神经元。

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