Nagata Y, Ando M, Hori S
Neurochem Res. 1985 Aug;10(8):1173-85. doi: 10.1007/BF00965890.
Effects of nerve growth factor (NGF) on the uptake of non-metabolizable alpha-aminoisobutyric acid (AIB) and on Na,K-ATPase activity in superior cervical sympathetic ganglia (SCG) excised from adult rats were examined during aerobic incubation in vitro. Active uptake of labelled AIB into isolated SCG during 1 to 5 hours incubation at 37 degrees C was significantly accelerated by the addition of NGF to the incubation medium in a dose-dependent manner. Although the Km value of the AIB uptake by the SCG did not change with the addition of NGF, Vmax was nearly doubled. The NGF-evoked increase in AIB uptake was antagonized by the further addition of its specific antiserum in a dose-dependent fashion, and was largely suppressed in a medium containing ouabain. In SCG, axotomized one week prior to the examination, from which most of the neurons had disappeared and reactive proliferation of satellite glial components was in progress, the NGF-induced acceleration of AIB uptake was completely absent. The ganglionic Na,K-ATPase activity was greatly stimulated in the presence of NGF, and the effect was completely eliminated in the axotomized SCG. These results strongly suggest that the NGF-induced acceleration of active AIB uptake by the isolated SCG occurs not in glial cells but exclusively in the neuronal components with the apparent coupling of an Na ion extrusion process.
在体外有氧孵育过程中，研究了神经生长因子（NGF）对成年大鼠切除的颈上神经节（SCG）摄取非代谢性α-氨基异丁酸（AIB）以及对Na，K-ATP酶活性的影响。在37℃孵育1至5小时期间，向孵育培养基中添加NGF以剂量依赖性方式显著加速了标记的AIB向分离的SCG中的主动摄取。尽管添加NGF后SCG摄取AIB的Km值没有变化，但Vmax几乎增加了一倍。进一步添加其特异性抗血清以剂量依赖性方式拮抗了NGF引起的AIB摄取增加，并且在含有哇巴因的培养基中大部分被抑制。在检查前一周进行轴突切断的SCG中，大部分神经元已经消失且卫星胶质细胞成分正在进行反应性增殖，完全不存在NGF诱导的AIB摄取加速。在存在NGF的情况下，神经节的Na，K-ATP酶活性受到极大刺激，并且在轴突切断的SCG中该作用完全消除。这些结果强烈表明，NGF诱导的分离的SCG对AIB的主动摄取加速不是发生在胶质细胞中，而是仅发生在神经元成分中，并且明显与Na离子挤出过程偶联。
