Guerra A, Urbina M, Lima L
Laboratorio de Neuroquímica, Centro de Biofísica y Bioquímica, Instituto Venezolano de Investigaciones Científicas, Caracas, Venezuela.
Amino Acids. 2000;19(3-4):687-703. doi: 10.1007/s007260070016.
Although there are a great number of studies concerning the uptake of taurine in several tissues, the regulation of taurine transport has not been studied in the retina after lesioning the optic nerve. In the present study, isolated retinal cells of the goldfish retina were used either immediatly after cell suspension or in culture. The high-affinity transport system of [3H]taurine in these cells was sodium-, temperature- and energy-dependent, and was inhibited by hypotaurine and beta-alanine, but not by gamma-aminobutyric acid. There was a decrease in the maximal velocity (Vmax) without modifications in the substrate affinity (Km) after optic axotomy. These changes were mantained for up to 15 days after the lesion. The results might be the summation of mechanisms for providing extracellular taurine to be taken up by other retinal cells or eye structures, or regulation by the substrate taurine, which increases after lesioning the optic nerve. The in vivo accumulation of [3H]taurine in the retina after intraocular injection of [3H]taurine was affected by crushing the optic nerve or by axotomy. A progressive retinal decrease in taurine transport was observed after crushing the optic nerve, starting at 7 hours after surgery on the nerve. The uptake of [3H]taurine by the tectum was compensated in the animals that were subjected to crushing of the optic nerve, since the concentration of [3H]taurine was only different from the control value 24 hours after the lesion, indicating an efficient transport by the remaining axons. On the contrary, the low levels of [3H]taurine in the tectum after axotomy might be an index of the non-axonal origin of taurine in the tectum. Axonal transport was illustrated by the differential presence of [3H]taurine in the intact or crushed optic nerve. The uptake of [3H]taurine into retinal cells in culture in the absence or in the presence of taurine might indicate the existence of an adaptive regulation of taurine transport in this tissue, however taurine transport probably differentially occurs in specific populations of retinal cells. The use of a purified preparation of cells might be useful for future studies on the modulation of taurine transport by taurine in the retina and its role during regeneration.
尽管有大量关于牛磺酸在多种组织中摄取的研究,但视神经损伤后视网膜中牛磺酸转运的调节尚未得到研究。在本研究中,金鱼视网膜的分离细胞在细胞悬浮后立即使用或用于培养。这些细胞中[3H]牛磺酸的高亲和力转运系统依赖于钠、温度和能量,并且被亚牛磺酸和β-丙氨酸抑制,但不被γ-氨基丁酸抑制。视神经切断术后,最大速度(Vmax)降低,而底物亲和力(Km)未改变。这些变化在损伤后长达15天内持续存在。结果可能是为其他视网膜细胞或眼结构提供细胞外牛磺酸以供摄取的机制的总和,或者是由底物牛磺酸调节的结果,牛磺酸在视神经损伤后会增加。眼内注射[3H]牛磺酸后,视网膜中[3H]牛磺酸的体内积累受到视神经挤压或切断的影响。视神经挤压后,从神经手术7小时开始,观察到视网膜中牛磺酸转运逐渐减少。视神经挤压的动物中,顶盖对[3H]牛磺酸的摄取得到了补偿,因为损伤后24小时[3H]牛磺酸的浓度才与对照值不同,这表明剩余轴突的转运效率较高。相反,切断术后顶盖中[3H]牛磺酸水平较低可能是顶盖中牛磺酸非轴突来源的一个指标。完整或挤压的视神经中[3H]牛磺酸的差异存在说明了轴突运输。在有或没有牛磺酸的情况下,[3H]牛磺酸在培养的视网膜细胞中的摄取可能表明该组织中牛磺酸转运存在适应性调节,然而牛磺酸转运可能在特定的视网膜细胞群体中存在差异。使用纯化的细胞制剂可能有助于未来研究牛磺酸对视网膜中牛磺酸转运的调节及其在再生过程中的作用。