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大鼠脊髓中多巴胺D1受体介导运动轴突侧支至闰绍细胞突触传递调节的证据。

Evidence for D1 dopamine receptor-mediated modulation of the synaptic transmission from motor axon collaterals to Renshaw cells in the rat spinal cord.

作者信息

Seth P, Gajendiran M, Maitra K K, Ross H G, Ganguly D K

机构信息

Division of Pharmacology and Experimental Therapeutics, Indian Institute of Chemical Biology, Calcutta.

出版信息

Neurosci Lett. 1993 Aug 20;158(2):217-20. doi: 10.1016/0304-3940(93)90268-p.

Abstract

The possible modulatory role of D1 dopamine receptors on the excitability of lumbar spinal Renshaw cells was studied in anesthetized rats spinalized at T4 level. Burst responses elicited by single electrical shocks to ipsilateral ventral roots L6 (frequency 0.5 Hz, stimulus width 0.1 ms) and spontaneous activity were recorded extracellularly using conventional 3 M KCl filled glass micropipettes. The specific D1 agonist SKF 38393 (0.5-1 mg/kg i.v.) enhanced Renshaw cell burst responses by 20-60% (n = 7) and increased their spontaneous discharge rate (n = 3). This effect was clearly antagonized by the specific D1 antagonist SCH 23390 (1 mg/kg i.v.) although SCH 23390 proved ineffective per se. We conclude that SKF 38393 induced facilitation was due to activation of the specific D1 receptors which could be the functional counterpart of the presynaptic D2 receptors described earlier by us in the same synapse.

摘要

在T4水平脊髓横断的麻醉大鼠中,研究了D1多巴胺受体对腰段脊髓闰绍细胞兴奋性的可能调节作用。使用常规的3M KCl填充玻璃微电极细胞外记录对同侧L6腹根进行单次电击(频率0.5Hz,刺激宽度0.1ms)引发的爆发反应和自发活动。特异性D1激动剂SKF 38393(0.5 - 1mg/kg静脉注射)使闰绍细胞爆发反应增强20 - 60%(n = 7),并增加其自发放电率(n = 3)。尽管特异性D1拮抗剂SCH 23390(1mg/kg静脉注射)本身无效,但该作用明显被其拮抗。我们得出结论,SKF 38393诱导的易化作用是由于特异性D1受体的激活,这可能是我们之前在同一突触中描述的突触前D2受体的功能对应物。

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