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Effects of Cerebral Ischemia on [ 3 H]Inositol Lipids and [ 3 H]Inositol Phosphates of Gerbil Brain and Subcellular Fractions
Author(s) -
Strosznajder Joanna,
Wikiel Hanna,
Sun Grace Y.
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb05608.x
Subject(s) - gerbil , inositol , phosphatidylinositol , pi , ischemia , chemistry , lithium (medication) , biochemistry , ligation , calcium , endocrinology , medicine , biology , receptor , signal transduction , organic chemistry
Intracerebral injection of [ 3 H]inositoi into gerbil brain resulted in labeling of phosphoinositides and inositolphosphates in various subcellular membrane fractions. Phosphatidylinositol (PI) comprised >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 trisphosphate (63%) and inositol bisphosphate (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.