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急性而非慢性乙醇处理对大鼠下丘脑神经元生长抑素分泌的影响。

Effect of acute, but not chronic ethanol treatment on somatostatin secretion in rat hypothalamic neurons.

作者信息

Rage F, Arancibia S, Tapia-Arancibia L

机构信息

Laboratoire de Plasticité Cérébrale, EP 628 CNRS, Université de Montpellier 2, France.

出版信息

Neurosci Lett. 1998 Apr 10;245(3):175-9. doi: 10.1016/s0304-3940(98)00199-2.

Abstract

To examine the possible involvement of somatostatin in growth hormone modifications induced by ethanol, we examined: (1) the effects of chronic ethanol exposure of cultured hypothalamic neurons on somatostatin content and mRNA levels; (2) the acute effect of ethanol on somatostatin release stimulated by N-methyl-D-aspartate (NMDA). The results showed that 8 days of ethanol exposure (10-100 mM) did not decrease somatostatin content or somatostatin mRNA levels. Ethanol treatment alone had no significant effect on cell morphology or on protein content. In contrast, acute application of ethanol in 8 day-old cultures significantly reduced (50 mM) or completely blocked (100 mM) somatostatin release elicited by 50 microM NMDA without modifying basal release. We conclude that chronic ethanol treatment to concentrations up to 100 mM has no effect on somatostatin biosynthesis in fetal rat hypothalamic neurons, while weaker concentrations decrease NMDA-induced somatostatin release.

摘要

为研究生长抑素是否可能参与乙醇诱导的生长激素变化,我们进行了以下研究:(1) 长期乙醇暴露对培养的下丘脑神经元中生长抑素含量和mRNA水平的影响;(2) 乙醇对N-甲基-D-天冬氨酸(NMDA)刺激的生长抑素释放的急性作用。结果显示,暴露于乙醇8天(10 - 100 mM)并未降低生长抑素含量或生长抑素mRNA水平。单独乙醇处理对细胞形态或蛋白质含量无显著影响。相反,在8日龄培养物中急性应用乙醇可显著降低(50 mM)或完全阻断(100 mM)由50 μM NMDA引发的生长抑素释放,而不改变基础释放。我们得出结论,浓度高达100 mM的慢性乙醇处理对胎鼠下丘脑神经元中生长抑素的生物合成无影响,而较低浓度会降低NMDA诱导的生长抑素释放。

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