Effect of chronic ethanol treatment and selective breeding for sensitivity to ethanol on calcium release induced by inositol trisphosphate or ethanol from brain and liver microsomes.
Effect of chronic ethanol treatment and selective breeding for sensitivity to ethanol on calcium release induced by inositol trisphosphate or ethanol from brain and liver microsomes.
复制标题
长期乙醇处理和乙醇敏感性选择性育种对肌醇三磷酸或乙醇诱导的脑和肝微粒体钙释放的影响。
DOI：
10.1111/j.1530-0277.1991.tb01860.x
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Harris,RA
中科院分区：
文献类型：
--
作者：
Daniell,LC;Harris,RA
我们以前的工作表明，乙醇增加了突触体中静息细胞内游离钙浓度（CA），并从脑微粒体的三磷酸肌醇（IP3）不敏感的钙储存中释放钙。在这份报告中，我们研究了慢性乙醇处理和选择性繁殖对乙醇催眠敏感性对IP 3和乙醇刺激的脑和肝微粒体钙释放的影响。长期乙醇处理未改变IP3刺激的脑微粒体钙释放或乙醇刺激的脑或肝微粒体钙释放。慢性乙醇处理增加了自发释放的钙从大脑，但不是肝微粒体。在从长睡眠（LS）和短睡眠（SS）小鼠的小脑或大脑皮层分离的微粒体中，乙醇和IP 3以浓度依赖性方式释放钙。乙醇和IP 3释放的钙量在小脑微粒体中大于大脑皮质微粒体。然而，乙醇和IP3释放的钙量在两条线或大脑区域之间没有差异。这些结果并不支持乙醇的催眠作用是由于乙醇诱导的脑组织中非线粒体细胞内钙储存的钙释放。乙醇耐受性和依赖性的发展似乎也与乙醇从非线粒体细胞内储存中释放钙的能力改变无关;然而，长期乙醇暴露对细胞内钙自发释放的影响可能会改变乙醇依赖性的神经元功能。
Our previous work showed that ethanol increases the resting intracellular free calcium concentration (CA,) in synaptosomes and releases calcium from an inositol trisphosphate (IP3)‐insensitive calcium store of brain microsomes. In this report, we investigated the effects of chronic ethanol treatment and selective breeding for hypnotic sensitivity to ethanol on IP3and ethanol‐stimulated calcium release from brain and liver microsomes. Chronic ethanol treatment did not alter IP3,‐stimulated calcium release from brain microsomes or ethanol‐stimulated calcium release from brain or liver microsomes. Chronic ethanol treatment increased the spontaneous release of calcium from brain but not liver microsomes. In microsomes isolated from cerebellum or cerebral cortex of long‐sleep (LS) and short‐sleep (SS) mice, ethanol and IP3released calcium in a concentration dependent manner. The amount of calcium released by ethanol and IP3was larger in microsomes isolated from cerebellum than microsomes from cerebral cortex. However, the amount of calcium released by ethanol and IP3did not differ between the two lineseither brain area. These results do not support the idea that the hypnotic effects of ethanol are due to ethanol‐induced calcium release from a nonmitochondrial intracellular calcium store in brain tissue. The development of ethanol tolerance and dependence also does not appear to be associated with altered ability of ethanol to release calcium from non‐mitochondrial intracellular stores; however, effects of chronic ethanol exposure on spontaneous release of intracellular calcium could alter neuronal function in ethanol dependence.