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青蛙的延髓-脊髓吲哚胺能通路。

The bulbo-spinal indoleaminergic pathway in the frog.

作者信息

Soller R W, Erulkar S D

出版信息

Brain Res. 1979 Aug 24;172(2):277-93. doi: 10.1016/0006-8993(79)90538-9.

DOI:10.1016/0006-8993(79)90538-9
PMID:223737
Abstract

The role of the bulbo-spinal indoleaminergic pathway of the frog was investigated. Using the isolated spinal cord preparation, responses of motoneurons of segments 9 and 10 to lateral column stimulation were recorded from ventral roots (LC-VRP) and by intracellularly placed microelectrodes. Control responses were compared to those obtained after addition of substances known to alter indoleaminergic synthesis or receptor activation. Responses from spinal cords of animals that were pretreated with indoleamine-depleting agents were compared to mean control responses. Procedures that inhibited indoleamine synthesis or blocked indoleamine receptors reduced motoneuronal activity. This was manifested as an increase in mean latency and a decrease in amplitude of the monosynaptic LC-VRP, an increased duration of suppression following an LC conditioning stimulus, and a decrease in spontaneous activity. In contrast to intracellularly recorded responses from control cords, those recorded under these conditions typically showed single spikes with longer latencies. Additions of indoleamine precursors to normal cords or to cords depleted of monoamines by reserpine shortened mean latencies, increased amplitudes of LC-elicited responses and caused an increase in spontaneous activity. These observations were recorded both extracellularly and intracellularly. Our results suggest that the bulbo-spinal indoleaminergic pathway modulates the output of motoneurons of the frog spinal cord.

摘要

研究了青蛙延髓 - 脊髓吲哚胺能通路的作用。使用离体脊髓标本,从腹根(LC - VRP)并通过细胞内放置的微电极记录第9和第10节段运动神经元对外侧柱刺激的反应。将对照反应与添加已知会改变吲哚胺能合成或受体激活的物质后获得的反应进行比较。将用吲哚胺消耗剂预处理的动物的脊髓反应与平均对照反应进行比较。抑制吲哚胺合成或阻断吲哚胺受体的程序会降低运动神经元的活性。这表现为单突触LC - VRP的平均潜伏期增加和幅度减小、LC条件刺激后抑制持续时间增加以及自发活动减少。与对照脊髓细胞内记录的反应相比,在这些条件下记录的反应通常显示潜伏期更长的单个峰电位。向正常脊髓或被利血平耗尽单胺的脊髓中添加吲哚胺前体可缩短平均潜伏期、增加LC引发反应的幅度并导致自发活动增加。这些观察结果通过细胞外和细胞内记录得到。我们的结果表明,延髓 - 脊髓吲哚胺能通路调节青蛙脊髓运动神经元的输出。

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