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红海鲀毒素使大鼠脑片释放的5-羟色胺和去甲肾上腺素增加。

Increased 5-hydroxytryptamine and norepinephrine release from rat brain slices by the Red Sea flatfish toxin pardaxin.

作者信息

Wang H Y, Friedman E

出版信息

J Neurochem. 1986 Aug;47(2):656-8. doi: 10.1111/j.1471-4159.1986.tb04550.x.

Abstract

The effect of the Red Sea flatfish toxin pardaxin was examined on K+-evoked and on basal release of either [3H]norepinephrine or [3H]5-hydroxytryptamine from preloaded rat cortical slices. The K+-induced release of the neurotransmitters was stimulated in a dose-related manner at concentrations ranging from 0.5 to 4 micrograms/ml. Basal release of the two transmitters was elevated to a lesser extent. Although the stimulation of evoked release was approximately equivalent for the two neurotransmitters, the response to 5-hydroxytryptamine was reversible whereas that of norepinephrine was not washed by 20 min of superfusion. The mechanisms involved in producing these actions of pardaxin are not known; however, they may be mediated by changes in electrolyte fluxes across the neuronal membranes.

摘要

研究了红海比目鱼毒素pardaxin对预加载的大鼠皮质切片中钾离子诱发的以及基础状态下[3H]去甲肾上腺素或[3H]5-羟色胺释放的影响。在浓度范围为0.5至4微克/毫升时,钾离子诱导的神经递质释放呈剂量相关方式受到刺激。两种神经递质的基础释放升高程度较小。尽管两种神经递质诱发释放的刺激作用大致相当,但对5-羟色胺的反应是可逆的,而去甲肾上腺素的反应在20分钟的灌流后并未被洗脱。产生pardaxin这些作用的机制尚不清楚;然而,它们可能是由跨神经元膜的电解质通量变化介导的。

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