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首页> 外文期刊>Life sciences >EFFECTS OF FLUOXETINE ON BASAL AND K+-INDUCED TRITIUM RELEASE FROM SYNAPTOSOMES PRELOADED WITH [H-3]SEROTONIN
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EFFECTS OF FLUOXETINE ON BASAL AND K+-INDUCED TRITIUM RELEASE FROM SYNAPTOSOMES PRELOADED WITH [H-3]SEROTONIN

机译：氟西汀对[H-3] 5-羟色胺预加载突触体基底和K +诱导的RIT释放的影响

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Synaptosomes from rat brain cortex and spinal cord were preloaded with [H-3]serotonin ([H-3]5-HT), superfused and exposed to fluoxetine and/or 15 mM K+. In both regions 10 mu M, but not 1 mu M fluoxetine evoked a marked tritium overflow, about 2 min later than the immediate [H-3]5-HT release induced by K+, and mainly (73%) due to the efflux of a tritiated metabolite of 5-HT, possibly [H-3]5-hydroxy-indoleacetic acid. These findings confirm previous data in the rat hippocampus and are probably due to fluoxetine interacting with the 5-HT storage vesicles. One mu M fluoxetine significantly reduced the d-fenfluramine-induced [H-3]5HT overflow, in accordance with its action as 5-HT uptake blocker, but did not affect the K+-induced [H-3]5-HT overflow. This latter finding does not confirm that fluoxetine inhibits the depolarization-induced Ca2+-influx, suggested to involve a drug interaction with the L-type Ca2+-channels. This, the overflow induced by 10 mu M fluoxetine was additive with the depolarization-induced overflow, when the two stimuli were applied together. When 10 mu M fluoxetine was added 7 min before 15 mM K+, there was no depolarization-induced overflow. Such inhibition might be only apparent and due either to the fluoxetine-induced loss of vesicular 5-HT or to a fluoxetine-induced alteration of synaptic vesicles. The in vivo relevance of the fluoxetine releasing effect remains to be assessed. [References: 21]
机译：在大鼠大脑皮层和脊髓的突触小体上预装[H-3]血清素（[H-3] 5-HT），进行融合并暴露于氟西汀和/或15 mM K +。在这两个区域中，10μM而非1μM氟西汀引起明显的tri溢出，比K +引起的立即[H-3] 5-HT释放晚约2分钟，主要是（73％）由于5-HT的tri代代谢物，可能是[H-3] 5-羟基-吲哚乙酸。这些发现证实了大鼠海马中的先前数据，可能是由于氟西汀与5-HT储存囊泡相互作用。根据其作为5-HT摄取阻滞剂的作用，一μM氟西汀可显着降低d-芬氟拉明诱导的[H-3] 5HT溢出，但不影响K +诱导的[H-3] 5-HT溢出。后一个发现并未证实氟西汀抑制去极化诱导的Ca2 +内流，提示其涉及与L型Ca2 +通道的药物相互作用。当将两种刺激物一起使用时，由10μM氟西汀引起的溢出与去极化引起的溢出相加。当在15 mM K +之前7分钟加入10μM氟西汀时，没有去极化诱导的上溢。这种抑制可能仅是明显的，并且是由于氟西汀诱导的5-HT囊泡损失或氟西汀诱导的突触小泡改变。氟西汀释放作用的体内相关性尚待评估。 [参考：21]

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