Deshpande S B, Warnick J E
Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore 21201.
Neurosci Lett. 1990 Aug 14;116(1-2):141-8. doi: 10.1016/0304-3940(90)90400-4.
The interaction between thyrotropin-releasing hormone (TRH) and methysergide (MeSG) on reflex activity was examined in spinal cords from neonatal rats. MeSG depressed the monosynaptic reflex (MSR) by nearly 90% at 0.03 microM but had no effect on the dorsal root reflex at 0.003-3.0 microM. Neither spiperone, ketanserin, cyproheptadine nor ICS 205-930 (3-tropanyl-indole-3-carboxylate) depressed the MSR nor did they affect the potentiation elicited by TRH. TRH reversed the depression of the MSR by MeSG in a concentration-dependent manner without affecting the dorsal root reflex. MeSG-induced depression of the MSR was also reversed by 3,4-diaminopyridine which simultaneously increased the magnitude and duration of both reflexes. It appears that neither MeSG-induced depression nor TRH-induced potentiation of the MSR involves the spinal serotonergic system or blockade of K+ channels.
在新生大鼠的脊髓中研究了促甲状腺激素释放激素（TRH）与麦角新碱（MeSG）对反射活动的相互作用。在0.03微摩尔浓度时，MeSG使单突触反射（MSR）降低了近90%，但在0.003 - 3.0微摩尔浓度时对背根反射无影响。舒必利、酮色林、赛庚啶和ICS 205 - 930（3 - 托烷 - 吲哚 - 3 - 羧酸）均未降低MSR，也未影响TRH引起的增强作用。TRH以浓度依赖的方式逆转了MeSG对MSR的抑制，且不影响背根反射。3,4 - 二氨基吡啶也逆转了MeSG引起的MSR抑制，同时增加了两种反射的幅度和持续时间。似乎MeSG引起的MSR抑制和TRH引起的MSR增强均不涉及脊髓5 - 羟色胺能系统或钾通道的阻断。
