Hoshino M, Asakura T, Matsuda M
J Nutr Sci Vitaminol (Tokyo). 1979;25(5):367-74. doi: 10.3177/jnsv.25.367.
The in vivo effect of semicarbazide (SC) and aminoxyacetic acid (AOAA) upon gamma-aminobutyric acid (GABA) levels in the synaptosomal fraction, and GABA release from the same fraction were studied in the mouse. The convulsive dose of SC reduced the GABA content in synaptosomes, and when the convulsions were protected by pretreatment with AOAA, the reduced GABA content in synaptosomes rose to or above the normal level. Moreover, the SC treatment decreased the GABA releases from synaptosomes both in a Ca2+-free Ringer's solution and in a high K+ Ringer's solution. When the convulsions were protected by pretreatment with AOAA, the decreased GABA releases in both the conditions rose to or above the normal levels. Therefore, it is suggested that the decrease in GABA release from the nerve endings, because of the decrease of GABA content in the same compartment, is possibly an important factor in the onset of some kinds of convulsions.
在小鼠中研究了氨基脲（SC）和氨氧基乙酸（AOAA）对突触体部分中γ-氨基丁酸（GABA）水平以及同一部分GABA释放的体内效应。SC的惊厥剂量降低了突触体中的GABA含量，当用AOAA预处理保护惊厥时，突触体中降低的GABA含量升至正常水平或以上。此外，SC处理在无Ca2+的林格氏液和高K+林格氏液中均降低了突触体的GABA释放。当用AOAA预处理保护惊厥时，两种情况下降低的GABA释放均升至正常水平或以上。因此，提示由于同一隔室中GABA含量的减少导致神经末梢GABA释放的减少可能是某些类型惊厥发作的重要因素。
