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Aging Diminishes Serotonin‐Stimulated Arachdonic Acid Uptake and Cholinergic Receptor‐Activated Arachidonic Acid Release in Rat Brain Cortex Membrane
Author(s) -
Strosznajder J.,
Samochocki M.,
Duran M.
Publication year - 1994
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 - 10.1046/j.1471-4159.1994.62031048.x
Subject(s) - endocrinology , medicine , synaptosome , arachidonic acid , receptor , chemistry , pargyline , postsynaptic potential , carbachol , cortex (anatomy) , serotonin , biology , biochemistry , neuroscience , central nervous system , enzyme
Synaptoneurosomal and synaptosomal fractions from the brain cortex of adult (4‐month‐old) and aged (27‐month‐old) rats were used for studies on the uptake and subsequent release of [ 14 C]arachidonic acid ([ 14 C]AA) from brain lipids. The incorporation of AA and the pattern of its uptake into lipids of the aged brain cortex synapto‐neurosomes and synaptosomes were not significantly different when compared with those in the adult brain cortex fractions. Serotonin (5‐HT), at 10 μM to 1 μM in the presence of pargyline and the agonist of the 5‐HT 1A receptor, buspirone, stimulated AA uptake into membrane lipids, mainly into phosphatidylinositol, by about 40% exclusively in adult brain synaptoneurosomes. Aging significantly diminished the effect of 5‐HT on AA uptake. Synaptoneurosomal and synaptosomal fractions prelabeled with [ 14 C]AA were used subsequently for investigation of voltage‐dependent, muscarinic and 5‐HT receptor‐mediated AA release. Aging diminished markedly carbachol‐stimulated Ca 2+ ‐dependent AA liberation from membrane lipids of synaptoneurosomes and synaptosomes. Moreover, aging decreased voltage‐dependent and 5‐HT 2 receptor‐mediated AA release. These results show that aging affects receptor‐dependent AA uptake and pre‐and postsynaptic receptor‐mediated AA release. These modulations of AA incorporation and release in aged brain may be of patho‐physiological significance, in view of the importance of these processes for signal transmission in the brain. The changes of receptor‐dependent processes of deacylation and reacylation may be responsible for alteration in the function of neuronal cells and may affect learning and memory ability and brain plasticity during aging.