Strosznajder J, Wikiel H, Sun G Y
J Neurochem. 1987 Mar;48(3):943-8. doi: 10.1111/j.1471-4159.1987.tb05608.x.
Intracerebral injection of [3H]inositol into gerbil brain resulted in labeling of phosphoinositides and inositol-phosphates in various subcellular membrane fractions. Phosphatidylinositol (PI) comprised greater than 90% of the radioactivity of inositol lipids. However, the level of labeled poly-PI (with respect to PI) was higher in synaptosomes than in other membrane fractions. Ischemia induced in gerbils by ligation of the common carotid arteries resulted in a 30% decrease in labeled poly-PI in brain homogenates and this decrease was largely attributed to the poly-PI in synaptosomes (50% decrease). Among the inositol phosphates, the ischemia induction resulted in a decrease in labeling of inositol triphosphate (63%) and inositol biphosphate (38%), but labeling of inositol phosphate (IP) was increased by 59%. The results suggested a rapid turnover of the inositol phosphates in the gerbil brain. In general, changes in inositol lipids and inositol phosphates due to ischemia were attenuated after pretreatment with lithium (3 meq/kg) injected intraperitoneally 5 h prior to ligation. Surprisingly, lithium treatment alone did not cause an increase in IP labeling in the gerbil brain.
向沙鼠脑内注射[3H]肌醇会导致各种亚细胞膜组分中的磷酸肌醇和肌醇磷酸被标记。磷脂酰肌醇（PI）占肌醇脂质放射性的90%以上。然而，突触体中标记的多磷酸肌醇（相对于PI）水平高于其他膜组分。通过结扎颈总动脉在沙鼠中诱导的缺血导致脑匀浆中标记的多磷酸肌醇减少30%，这种减少主要归因于突触体中的多磷酸肌醇（减少50%）。在肌醇磷酸中，缺血诱导导致肌醇三磷酸（63%）和肌醇二磷酸（38%）的标记减少，但肌醇磷酸（IP）的标记增加了59%。结果表明沙鼠脑中肌醇磷酸有快速周转。一般来说，在结扎前5小时腹腔注射锂（3 meq/kg）预处理后，缺血引起的肌醇脂质和肌醇磷酸的变化会减弱。令人惊讶的是，单独锂处理并未导致沙鼠脑中IP标记增加。
