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牛磺酸与钠协同转运导致神经元膜去极化。

Depolarization of the neuronal membrane caused by cotransport of taurine and sodium.

作者信息

Holopainen I, Lidén E, Nilsson A, Sellström A

机构信息

Department of Biomedical Sciences, University of Tampere, Finland.

出版信息

Neurochem Res. 1990 Jan;15(1):89-94. doi: 10.1007/BF00969189.

Abstract

C 1300 neuroblastoma cells were cultured and used to study the effect of sodium dependent taurine transport on the membrane potential. Measuring net accumulation of taurine and the depolarization caused by externally applied taurine, we found both processes become active at an external concentration of taurine of 1 mM or more. Net accumulation had Km of 13 mM and a Vmax of 126 nmol x mg of protein-1 x min-1. The taurine induced depolarization of the neuroblastoma cell was parallelled by a 25 per cent decrease in its membrane impedance. The transport of taurine, the depolarization caused by taurine and the effect of taurine on the membrane impedance, all, had a similar dependence on the external sodium concentration. Our results on the depolarizing cotransport between taurine and sodium at the neuronal membrane, may illustrate an additional mechanism for the control of the electrical activity of neuronal cells.

摘要

培养1300个神经母细胞瘤细胞,用于研究钠依赖性牛磺酸转运对膜电位的影响。通过测量牛磺酸的净积累量以及外源性牛磺酸引起的去极化,我们发现当外部牛磺酸浓度达到1 mM或更高时,这两个过程都会变得活跃。净积累的米氏常数(Km)为13 mM,最大反应速度(Vmax)为126 nmol·mg蛋白质⁻¹·min⁻¹。牛磺酸诱导的神经母细胞瘤细胞去极化伴随着其膜阻抗降低25%。牛磺酸的转运、牛磺酸引起的去极化以及牛磺酸对膜阻抗的影响,都对外部钠浓度有类似的依赖性。我们关于神经元膜上牛磺酸与钠之间去极化协同转运的结果,可能阐明了一种控制神经元细胞电活动的额外机制。

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