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血清素增强大鼠脊髓背角浅层神经元对γ-氨基丁酸的反应。

Serotonin potentiates the response of neurons of the superficial laminae of the rat spinal dorsal horn to gamma-aminobutyric acid.

作者信息

Li H, Lang B, Kang J F, Li Y Q

机构信息

Department of Anatomy and K. K. Leung Brain Research Centre, The Fourth Military Medical University, People's Republic of, Xi'an, China.

出版信息

Brain Res Bull. 2000 Aug;52(6):559-65. doi: 10.1016/s0361-9230(00)00297-5.

DOI:10.1016/s0361-9230(00)00297-5
PMID:10974497
Abstract

Employing the Nystatin-perforated whole-cell patch-clamp recording technique, the modulatory effects of serotonin (5-HT) on gamma-aminobutyric acid (GABA)-activated whole-cell currents were investigated in neurons acutely dissociated from the superficial laminae (laminae I and II) of the rat spinal dorsal horn. The results showed: (1) GABA acted on GABA(A) receptors and elicited inward Cl(-) currents (I(GABA)) at a holding potential (V(H)) of -40 mV; (2) 5-HT potentiated GABA-induced Cl(-) current without affecting the reversal potential of I(GABA) and the apparent affinity of GABA to its receptor; (3) alpha-methyl-5-HT, a selective agonist of 5-HT(2) receptor, mimicked the potentiation effect of 5-HT on I(GABA), whereas ketanserine, an antagonist of 5-HT(2) receptor, blocked the potentiation effect of 5-HT; (4) Chelerythrine, an inhibitor of protein kinase C, reduced the potentiation effect of 5-HT on I(GABA). The present results indicate: (1) The potentiation of 5-HT on I(GABA) is mediated by 5-HT(2) receptor and through a protein kinase-dependent transduction pathway; (2) The interactions between 5-HT and GABA might play an important role in the modulation of nociceptive information transmission at spinal cord level.

摘要

采用制霉菌素穿孔全细胞膜片钳记录技术,在急性分离的大鼠脊髓背角浅层(Ⅰ层和Ⅱ层)神经元中研究了5-羟色胺(5-HT)对γ-氨基丁酸(GABA)激活的全细胞电流的调制作用。结果显示:(1)在-40 mV的钳制电位(V(H))下,GABA作用于GABA(A)受体并引发内向Cl(-)电流(I(GABA));(2)5-HT增强GABA诱导的Cl(-)电流,而不影响I(GABA)的翻转电位以及GABA与其受体的表观亲和力;(3)5-HT(2)受体的选择性激动剂α-甲基-5-HT模拟了5-HT对I(GABA)的增强作用,而5-HT(2)受体拮抗剂酮色林则阻断了5-HT的增强作用;(4)蛋白激酶C抑制剂白屈菜红碱降低了5-HT对I(GABA)的增强作用。本研究结果表明:(1)5-HT对I(GABA)的增强作用是由5-HT(2)受体介导并通过蛋白激酶依赖的转导途径实现的;(2)5-HT与GABA之间的相互作用可能在脊髓水平伤害性信息传递的调制中发挥重要作用。

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