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Ischemic Modification of Cerebrocortical Membranes: 5‐Hydroxytryptamine Receptors, Fluidity, and Inducible In Vitro Lipid Peroxidation
Author(s) -
Villacara A.,
Kumami K.,
Yamamoto T.,
Mrsulja B. B.,
Spatz M.
Publication year - 1989
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.1471-4159.1989.tb07375.x
Subject(s) - lipid peroxidation , in vitro , membrane fluidity , chemistry , receptor , 5 ht receptor , membrane , biochemistry , serotonin , neuroscience , biophysics , microbiology and biotechnology , biology , oxidative stress
The effect of ischemia on the properties of 5‐hydroxytryptamine 1A+B (5‐HT 1A+B ) and 5‐hydroxytrypt‐amine 1B 5‐HT 1B ) binding sites, physical‐state “fluidity” of the membrane, and its susceptibility to peroxidation in vitro was investigated in the cerebral cortex of gerbils. Ischemia was induced by bilateral carotid artery occlusion for 15 min alone or with release for 1 h. Ischemia both with and without reflow decreased the number of 5‐HT 1A+B and 5‐HT 1B binding sites, whereas ischemia and reflow altered the affinity for 5‐HT 1B binding sites. Resistance to the temperature‐dependent increase in “fluidity” of the membrane was detected (by fluorescence anisotropy using l,6‐diphenyl‐l,3,5‐hexatriene as a probe) after ischemia and reflow but not in ischemia alone. Susceptibility of the membranes to Fe 2+ ‐ and ascorbic acid‐stimulated lipid peroxidation in vitro was decreased following ischemia and recirculation only. These findings strongly suggest that the composition and the function of the membrane are markedly disturbed during recirculation after ischemia.