Segmental synaptic depression caused by diisopropylphosphorofluoridate and sarin is reversed by thyrotropin-releasing hormone in the neonatal rat spinal cord.
Segmental synaptic depression caused by diisopropylphosphorofluoridate and sarin is reversed by thyrotropin-releasing hormone in the neonatal rat spinal cord.
复制标题
由二异丙基氟磷酸酯和沙林引起的节段性突触抑制可被新生大鼠脊髓中的促甲状腺激素释放激素逆转。
DOI：
10.1016/0041-008x(88)90368-7
复制
发表时间：
1988
影响因子：
3.8
通讯作者：
Warnick,JE
中科院分区：
文献类型：
--
作者：
DasGupta,S;Deshpande,SB;Warnick,JE
The organophosphorus compounds diisopropylphosphorofluoridate (DFP) and isopropylmethyl-phosphonofluoridate (sarin) depressed the monosynaptic reflex (MSR) in spinal cords from 7- to 9-day-old male rats. The concentrations of DFP and sarin which depressed the MSR by nearly 50% were 100 μm and 100 nm, respectively. Simultaneous superfusion of the cords with thyrotropin-releasing hormone (TRH) with either DFP or sarin resulted in a reversal of the depression. The depression caused by DFP was reversed to 95% of control by 100 nm TRH whereas similar reversal of sarin-induced depression required a 10-fold greater concentration of TRH. The potentiating effect of TRH was not affected by atropine even at a high concentration (1 μm) although atropine easily reversed organophosphorus-induced depression of the MSR. It appears that reversal of organophosphorus-induced depression by TRH might occur through a noncholinergic, TRH-sensitive receptor mechanism and may be unrelated to acetylcholinesterase activity. This action represents a possible utility of TRH as an adjunct in organophosphorus toxicity.
