Singh A K, Banister E W
Can J Physiol Pharmacol. 1978 Apr;56(2):334-6. doi: 10.1139/y78-051.
Effects of 6-hydroxydopamine (6-OHDA) on rat brain and blood adrenaline (A), noradrenaline (NA), ammonia (NH3), gamma-aminobutyric acid (GABA), and amino acid metabolism prior to and after high pressure oxygen (OHP) induced convulsions have been studied. 6-OHDA reduces GABA and glutamate (Glu) rior to OHP exposure in rat brain so that the concentration is even equal to that seen in nondrugged animals after convulsion. Concomitantly, 6-OHDA reduces the latency of OHP-induced convulsion significantly, and increases brain NH3, glutamine, and asparagine significantly. Although 6-OHDA, in increasing dosage, elevates blood A concentration, convulsion produces a significant further increase in A. Blood NA was not significantly changed in drugged, convulsed animals and was much less than blood NA concentrations in nondrugged convulsed animals. Increasing doses of 6-OHDA also increase NH3 in the blood significantly and convulsion increases its concentration further. Latency of convulsion seems to be related to certain monoamine levels since in some drugged animals where A and total catecholamines are still reduced 96 h after the first of two doses of 6-OHDA, NA concentrations are recovered to relatively normal and the convulsion latency time is also increased although it remains significantly abbreviated from undrugged animals' convulsion time. Low brain GABA levels seem to be a prime effector of convulsive activity.
研究了6-羟基多巴胺(6-OHDA)对大鼠脑及血液中肾上腺素(A)、去甲肾上腺素(NA)、氨(NH3)、γ-氨基丁酸(GABA)以及高压氧(OHP)诱导惊厥前后氨基酸代谢的影响。在大鼠脑内,6-OHDA在OHP暴露前会降低GABA和谷氨酸(Glu)水平,使得其浓度甚至等同于未用药动物惊厥后的浓度。与此同时,6-OHDA显著缩短了OHP诱导惊厥的潜伏期,并显著增加了脑内NH3、谷氨酰胺和天冬酰胺的含量。尽管随着6-OHDA剂量增加,血液中A浓度升高,但惊厥会使A进一步显著增加。在用药且惊厥的动物中,血液NA无显著变化,且远低于未用药惊厥动物的血液NA浓度。6-OHDA剂量增加也会使血液中NH3显著增加,惊厥会使其浓度进一步升高。惊厥潜伏期似乎与某些单胺水平有关,因为在一些用药动物中,在给予两剂6-OHDA中的第一剂96小时后,A和总儿茶酚胺仍降低,但NA浓度恢复到相对正常水平,惊厥潜伏期也增加了,尽管仍显著短于未用药动物的惊厥时间。脑内低水平的GABA似乎是惊厥活动的主要影响因素。