Effects of cerebral ischemia on [3H]inositol lipids and [3H]inositol phosphates of gerbil brain and subcellular fractions.

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.