Ando M, Nagata Y
J Neurochem. 1986 May;46(5):1487-92. doi: 10.1111/j.1471-4159.1986.tb01766.x.
Active uptake of a labelled nonmetabolizable amino acid, alpha-aminoisobutyric acid (AIB), into isolated superior cervical sympathetic ganglia (SCG) excised from adult rats was considerably stimulated by the addition of either norepinephrine (NE, 50 microM) or 3,4-dihydroxyphenylethylamine (dopamine, DA, 100 microM) to the medium during aerobic incubation for 2 h at 37 degrees C. The NE-induced increase in AIB uptake was significantly antagonized by the addition of an alpha 1-adrenoceptor antagonist (prazosin, 10 microM) in SCG axotomized 1 week prior to the examination, in which most of the ganglionic neurons had degenerated and reactive proliferation of the satellite glial components was in progress. The addition of neither acetylcholine (ACh, 1 mM) plus eserine (0.1 mM) nor cyclic nucleotides (1 mM) changed the AIB uptake by the SCG. In the axotomized SCG, the NE-evoked increase in AIB uptake was much more pronounced than that of intact or denervated SCG. A kinetic study of the active AIB uptake in the SCG showed that NE produced a decrease of the Km value and an increase in the Vmax, especially in the axotomized SCG. Ganglionic Na+, K+-ATPase activity was greatly stimulated in the presence of NE, but not by ACh. These results strongly suggest that the NE-induced enhancement of active AIB uptake in the isolated SCG is occurring in glial cells rather than in neuronal cells, with a possible alteration of membrane properties for amino acid uptake and with an apparent regulation by the stimulated transport enzyme Na+, K+-ATPase.
在37℃有氧孵育2小时期间，向培养基中添加去甲肾上腺素（NE，50微摩尔）或3,4 - 二羟基苯乙胺（多巴胺，DA，100微摩尔），可显著刺激从成年大鼠分离出的颈上神经节（SCG）对标记的不可代谢氨基酸α-氨基异丁酸（AIB）的主动摄取。在检查前1周进行轴突切断的SCG中，添加α1 - 肾上腺素能受体拮抗剂（哌唑嗪，10微摩尔）可显著拮抗NE诱导的AIB摄取增加，此时大多数神经节神经元已退化，卫星胶质细胞成分正在进行反应性增殖。添加乙酰胆碱（ACh，1毫摩尔）加毒扁豆碱（0.1毫摩尔）或环核苷酸（1毫摩尔）均未改变SCG对AIB的摄取。在轴突切断的SCG中，NE引起的AIB摄取增加比完整或去神经支配的SCG更明显。对SCG中AIB主动摄取的动力学研究表明，NE导致Km值降低和Vmax增加，尤其是在轴突切断的SCG中。在NE存在下，神经节Na +，K + - ATP酶活性受到极大刺激，但ACh则不然。这些结果强烈表明，在分离的SCG中，NE诱导的AIB主动摄取增强发生在胶质细胞而非神经元细胞中，可能伴随着氨基酸摄取膜特性的改变以及受刺激的转运酶Na +，K + - ATP酶的明显调节。
