Strosznajder J, Samochocki M, Duran M
Laboratory of Cellular Signalling, Polish Academy of Sciences, Warsaw.
J Neurochem. 1994 Mar;62(3):1048-54. doi: 10.1046/j.1471-4159.1994.62031048.x.
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 [14C]arachidonic acid ([14C]AA) from brain lipids. The incorporation of AA and the pattern of its uptake into lipids of the aged brain cortex synaptoneurosomes and synaptosomes were not significantly different when compared with those in the adult brain cortex fractions. Serotonin (5-HT), at 10 microM to 1 mM in the presence of pargyline and the agonist of the 5-HT1A 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 [14C]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-HT2 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 pathophysiological 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.
来自成年（4个月大）和老年（27个月大）大鼠大脑皮层的突触神经小体和突触体组分，被用于研究[14C]花生四烯酸（[14C]AA）从脑脂质中的摄取及随后的释放。与成年大脑皮层组分相比，老年大脑皮层突触神经小体和突触体中AA的掺入及其摄取到脂质中的模式没有显著差异。在存在优降宁和5-HT1A受体激动剂丁螺环酮的情况下，10 microM至1 mM的血清素（5-HT）刺激AA摄取到膜脂质中，主要是磷脂酰肌醇，仅在成年大脑突触神经小体中增加约40%。衰老显著减弱了5-HT对AA摄取的影响。随后，用[14C]AA预标记的突触神经小体和突触体组分用于研究电压依赖性、毒蕈碱和5-HT受体介导的AA释放。衰老显著减少了卡巴胆碱刺激的突触神经小体和突触体膜脂质中Ca(2+)依赖性AA的释放。此外，衰老降低了电压依赖性和5-HT2受体介导的AA释放。这些结果表明，衰老影响受体依赖性AA摄取以及突触前和突触后受体介导的AA释放。鉴于这些过程对大脑信号传递的重要性，老年大脑中AA掺入和释放的这些调节可能具有病理生理学意义。受体依赖性去酰化和再酰化过程的变化可能是神经元细胞功能改变的原因，并可能影响衰老过程中的学习和记忆能力以及大脑可塑性。
