Fykse E M, Fonnum F
Division for Environmental Toxicology, Norwegian Defence Research Establishment, Kjeller.
J Neurochem. 1988 Apr;50(4):1237-42. doi: 10.1111/j.1471-4159.1988.tb10599.x.
Gamma-Aminobutyric acid (GABA) was taken up by a MgATP-dependent mechanism into synaptic vesicles isolated by hypoosmotic shock and density gradient centrifugation. The properties of the vesicular uptake differed clearly from those of synaptosomal and glial uptake, both with respect to Na+, Mg2+, and ATP dependence and with respect to response to general GABA uptake inhibitors such as nipecotic acid, diaminobutyric acid, and beta-alanine. The uptake showed a Km of 5.6 mM and a net uptake rate of 1,500 pmol/min/mg of protein. It is suggested that the vesicular uptake of GABA is driven by an electrochemical proton gradient generated by a Mg2+-ATPase.
γ-氨基丁酸(GABA)通过一种依赖MgATP的机制被摄取到经低渗休克和密度梯度离心分离得到的突触小泡中。囊泡摄取的特性在Na⁺、Mg²⁺和ATP依赖性方面,以及对一般GABA摄取抑制剂(如哌啶酸、二氨基丁酸和β-丙氨酸)的反应方面,都明显不同于突触体和胶质细胞的摄取。摄取显示出5.6 mM的Km值和1500 pmol/分钟/毫克蛋白质的净摄取率。有人提出,GABA的囊泡摄取是由Mg²⁺-ATP酶产生的电化学质子梯度驱动的。