Nakamura J, Mine K, Yamada S
Department of Neuropsychiatry, Kurume University, School of Medicine, Japan.
Kurume Med J. 1990;37(4):253-9. doi: 10.2739/kurumemedj.37.253.
A cannula was chronically implanted in the rat ventriculus, and anticonvulsants were administered through the cannula. The effects of the anticonvulsants applied, intraventricully, were investigated on the decreased electroconvulsive threshold induced by pretreatment with alpha-methyl-p-tyrosine (alpha-MT), p-chlorophenylalanine (PCPA) or allylglycine. The TRH analog, DN-1417, valproate (VPA), and phenobarbital (PB) raised the electroconvulsive threshold which had been lowered by alpha-MT. The reduced electroconvulsive threshold from PCPA was raised by DN-1417, but not by VPA or PB. The allylglycine induced lowering of the electroconvulsive threshold was raised by VPA and PB, but not by DN-1417. Phenytoin had no anticonvulsant effect on rats pretreated with these drugs. From these results, it was concluded that the anticonvulsant action of DN-1417 could be due to enhancement of dopamine and/or serotonin turnover.
将一根套管长期植入大鼠脑室，并通过该套管给予抗惊厥药。研究了经脑室给予的抗惊厥药对由α-甲基对酪氨酸（α-MT）、对氯苯丙氨酸（PCPA）或烯丙基甘氨酸预处理诱导的电惊厥阈值降低的影响。促甲状腺激素释放激素类似物DN-1417、丙戊酸盐（VPA）和苯巴比妥（PB）提高了由α-MT降低的电惊厥阈值。DN-1417提高了由PCPA降低的电惊厥阈值，但VPA或PB没有。VPA和PB提高了由烯丙基甘氨酸诱导降低的电惊厥阈值，但DN-1417没有。苯妥英对用这些药物预处理的大鼠没有抗惊厥作用。从这些结果得出结论，DN-1417的抗惊厥作用可能是由于多巴胺和/或血清素周转的增强。
