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大鼠视网膜P2亚细胞组分中[3H]牛磺酸的自发释放和诱发释放。

Spontaneous and evoked release of [3H]taurine from a P2 subcellular fraction of the rat retina.

作者信息

Lombardini J B

机构信息

Department of Pharmacology, Texas Tech University Health Sciences Center, Lubbock 79430.

出版信息

Neurochem Res. 1993 Feb;18(2):193-202. doi: 10.1007/BF01474684.

Abstract

The effects of spontaneous and evoked [3H]taurine release from a P2 fraction prepared from rat retinas were studied. The P2 fraction was preloaded with [3H]taurine under conditions of high-affinity uptake and then examined for [3H]taurine efflux utilizing superfusion techniques. Exposure of the P2 fraction to high K+ (56 mM) evoked a Ca(2+)-independent release of [3H]taurine. Li+ (56 mM) and veratridine (100 microM) had significantly less effect (8-15% and 15-30%, respectively) on releasing [3H]taurine compared to the K(+)-evoked release. 4-Aminopyridine (1 mM) had no effect on the release of [3H]taurine. The spontaneous release of [3H]taurine was also Ca(2+)-independent. When Na+ was omitted from the incubation medium K(+)-evoked [3H]taurine release was inhibited by approximately 40% at the first 5 minute depolarization period but was not affected at a second subsequent 5 minute depolarization period. The spontaneous release of [3H]taurine was inhibited by 60% in the absence of Na+. Substitution of Br- for Cl- had no effect on the release of either spontaneous or K(+)-evoked [3H]taurine release. However, substitution of the Cl- with acetate, isethionate, or gluconate decreased K(+)-evoked [3H]taurine release. Addition of taurine to the superfusion medium (homoexchange) resulted in no significant increase in [3H]taurine efflux. The taurine-transport inhibitor guanidinoethanesulfonic acid increased the spontaneous release of [3H]taurine by approximately 40%. These results suggest that the taurine release of [3H]taurine is not simply a reversal of the carrier-mediated uptake system. It also appears that taurine is not released from vesicles within the synaptosomes but does not rule out the possibility that taurine is a neurotransmitter. The data involving chloride substitution with permeant and impermeant anions support the concept that the major portion of [3H]taurine release is due to an osmoregulatory action of taurine while depolarization accounts for only a small portion of [3H]taurine release.

摘要

研究了从大鼠视网膜制备的P2组分中[3H]牛磺酸的自发释放和诱发释放的影响。P2组分在高亲和力摄取条件下预先加载[3H]牛磺酸,然后利用灌流技术检测[3H]牛磺酸的流出。将P2组分暴露于高钾(56 mM)会诱发[3H]牛磺酸的钙非依赖性释放。与钾诱发的释放相比,锂(56 mM)和藜芦碱(100 microM)对[3H]牛磺酸释放的影响明显较小(分别为8 - 15%和15 - 30%)。4 - 氨基吡啶(1 mM)对[3H]牛磺酸的释放没有影响。[3H]牛磺酸的自发释放也是钙非依赖性的。当孵育培养基中省略钠离子时,钾诱发的[3H]牛磺酸释放在第一个5分钟去极化期被抑制约40%,但在随后的第二个5分钟去极化期不受影响。在没有钠离子的情况下,[3H]牛磺酸的自发释放被抑制60%。用溴离子替代氯离子对自发或钾诱发的[3H]牛磺酸释放均无影响。然而,用醋酸根、羟乙基磺酸根或葡萄糖酸根替代氯离子会降低钾诱发的[3H]牛磺酸释放。向灌流培养基中添加牛磺酸(同源交换)导致[3H]牛磺酸流出没有显著增加。牛磺酸转运抑制剂胍基乙磺酸使[3H]牛磺酸的自发释放增加约40%。这些结果表明,[3H]牛磺酸的牛磺酸释放并非简单地是载体介导摄取系统的逆转。似乎牛磺酸也不是从突触小体中的囊泡释放的,但并不排除牛磺酸是神经递质的可能性。涉及用渗透性和非渗透性阴离子替代氯离子的数据支持这样的概念,即[3H]牛磺酸释放的主要部分是由于牛磺酸的渗透调节作用,而去极化仅占[3H]牛磺酸释放的一小部分。

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