Strosznajder J, Samochocki M, Duran M
Laboratory of Cellular Signalling, Polish Academy of Sciences, Warsaw.
Neurochem Int. 1994 Aug;25(2):193-9. doi: 10.1016/0197-0186(94)90039-6.
Brain cortex synaptoneurosomes actively incorporated [14C]arachidonic acid (AA) into lipids. Serotonin (5-HT), at a concentration range of 10 microM-1 mM, significantly stimulates the incorporation of AA mainly into phosphatidylinositol (PI) of brain cortex synaptoneurosomes. The stimulation rate of AA incorporation by 5-HT was the same in the presence and absence of lysophosphatidylinositol (LPI). However, in the absence of LPI some stimulation of AA uptake was also observed into phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid. Buspirone, an agonist of 5-HT1A receptor, has a similar effect on AA incorporation into membrane lipids as serotonin itself. Moreover, ketanserin, an antagonist of 5-HT2 receptor, also induces activation of AA incorporation into membrane lipids. On the other hand, glutamate, in a concentration dependent manner, significantly inhibits AA uptake into PI and also has some inhibitory action on AA uptake into the other lipids. Serotonin itself and the agonist of 5-HT1A receptor through the activation of AA turnover counteract glutamate-induced inhibition of AA uptake into lipids of brain cortex. Our results indicated that serotonin directly, through the specific receptors, or indirectly, through the interaction with glutamatergic receptors, modulates turnover and the level of arachidonic acid in the brain.
大脑皮层突触神经小体可将[14C]花生四烯酸(AA)主动掺入脂质中。血清素(5-羟色胺,5-HT)在10微摩尔至1毫摩尔的浓度范围内,能显著刺激AA主要掺入大脑皮层突触神经小体的磷脂酰肌醇(PI)中。在有和没有溶血磷脂酰肌醇(LPI)的情况下,5-HT对AA掺入的刺激率相同。然而,在没有LPI的情况下,也观察到AA对磷脂酰胆碱、磷脂酰乙醇胺和磷脂酸的摄取有一定刺激作用。5-HT1A受体激动剂丁螺环酮对AA掺入膜脂质的作用与血清素本身相似。此外,5-HT2受体拮抗剂酮色林也能诱导AA掺入膜脂质的激活。另一方面,谷氨酸以浓度依赖的方式显著抑制AA摄取到PI中,并且对AA摄取到其他脂质中也有一定抑制作用。血清素本身和5-HT1A受体激动剂通过激活AA周转抵消了谷氨酸诱导的大脑皮层脂质中AA摄取的抑制作用。我们的结果表明,血清素直接通过特定受体,或间接通过与谷氨酸能受体相互作用,调节大脑中花生四烯酸的周转和水平。