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Lesions to the Corticostriatal Pathways Ameliorate Hypoglycemia‐Induced Arachidonic Acid Release
Author(s) -
Westerberg Eva,
Wieloch Tadeusz
Publication year - 1986
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.1471-4159.1986.tb00786.x
Subject(s) - arachidonic acid , stearic acid , medicine , endocrinology , oleic acid , chemistry , palmitic acid , hypoglycemia , striatum , lesion , phosphatidylinositol , phospholipid , biochemistry , fatty acid , insulin , biology , enzyme , dopamine , surgery , organic chemistry , kinase , membrane
The concentrations of free fatty acids (FFAs) in the neostriatum of control rats and rats subjected to unilateral cortical ablation were measured during and following severe insulin‐induced hypoglycemia. The total FFA concentration in the caudate nucleus contralateral to the lesion increased to approximately 1.5 and 3 times the control level after 5 and 30 min of isoelectricity, respectively, and was similar to the control value following 1 h of recovery. After 5 min of isoelectricity, the total FFA pool was significantly smaller in the decorticated striatum. No difference between hemispheres was noted after 30 min of isoelectricity. After 5 min of isoelectricity the levels of stearic and arachidonic acid were selectively increased whereas palmitic acid and oleic acid remained at control levels. In the decorticated striatum of lesioned animals the arachidonic acid concentration was significantly lower, whereas the level of stearic acid was not significantly different from the control value. After 30 min of isoelectricity the levels of all four FFA species were increased. Apart from a significantly lower level of oleic acid on the decorticated side, there were no interhemi‐spheric differences in the FFA levels. Since the early inter‐hemispheric differences in the levels of arachidonic and stearic acids coincide with a selective decrease in the levels of glutamate and a decreased energy utilization on the decorticated side, the results suggest that glutamate release during hypoglycemia induces an early receptor‐mediated degradation of phospholipids, presumably via the phospha‐tidylinositol cycle.