Paul V, Krishnamoorthy M S
Department of Pharmacology & Environmental Toxicology, Dr. A. L. M. Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani.
Indian J Physiol Pharmacol. 1990 Apr;34(2):139-42.
Pretreatment with 5-hydroxytryptophan (5-HTP), a precursor of 5-HT, antagonised while pretreatment with p-chlorophenylalanine (PCPA), a 5-HT depletor, potentiated the myoclonus induced by picrotoxin, a GABA antagonist. Pretreatment with aminooxyacetic acid (AOAA), a GABA transaminase inhibitor, antagonised picrotoxin-induced myoclonus. The combined effect of the least protective doses of AOAA and 5-HTP was greater than the sum of their individual inhibitory effects on picrotoxin-induced myoclonus. Further, AOAA failed to inhibit picrotoxin-induced myoclonus in PCPA pretreated rats. These findings suggest that the central 5-HT-ergic system exerts a facilitatory influence on the GABA-ergic system and thus it is involved in the antimyoclonic action of GABA.
5-羟色氨酸(5-HTP)是5-羟色胺(5-HT)的前体,用其进行预处理可对抗由GABA拮抗剂印防己毒素诱导的肌阵挛,而用5-羟色胺耗竭剂对氯苯丙氨酸(PCPA)进行预处理则会增强该肌阵挛。用γ-氨基丁酸转氨酶抑制剂氨氧乙酸(AOAA)进行预处理可对抗印防己毒素诱导的肌阵挛。AOAA和5-HTP的最小保护剂量的联合作用大于它们各自对印防己毒素诱导的肌阵挛的抑制作用之和。此外,AOAA未能抑制PCPA预处理大鼠中由印防己毒素诱导的肌阵挛。这些发现表明,中枢5-羟色胺能系统对γ-氨基丁酸能系统发挥促进作用,因此它参与了γ-氨基丁酸的抗肌阵挛作用。