Felder C C, Kanterman R Y, Ma A L, Axelrod J
Section on Pharmacology, National Institute of Mental Health, Howard Hughes Medical Institute-National Institutes of Health Research Scholars Program, Bethesda, MD 20892.
Proc Natl Acad Sci U S A. 1990 Mar;87(6):2187-91. doi: 10.1073/pnas.87.6.2187.
Serotonin (5-HT) stimulated the release of arachidonic acid in hippocampal neurons cocultured with glial cells but not in glial cultures alone. Similar results were observed for the 5-HT-stimulated release of inositol phosphates. These results suggest a neural but not glial origin of both responses. Pharmacological studies suggested that release of arachidonic acid and inositol phosphates was mediated by a type 2 5-HT (5-HT2) receptor. 5-HT-stimulated release of arachidonic acid was also detected in cortical neurons, which contain high levels of 5-HT2 receptors, but not striatum, spinal cord, or cerebellar granule cells, which have very low levels or are devoid of 5-HT2 receptors. The phorbol ester phorbol 12-myristate 13-acetate augmented the 5-HT-stimulated release of arachidonic acid but inhibited the 5-HT-stimulated release of inositol phosphates. 5-HT-stimulated release of arachidonic acid, but not inositol phosphates, was dependent on extracellular calcium. 5-HT stimulated the release of [3H]lysophosphatidylcholine from [3H]choline-labeled cells with no increase in the release of [3H]choline or phospho[3H]choline. These data suggest that 5-HT stimulated the release of arachidonic acid in hippocampal neurons through the activation of phospholipase A2, independent of the activation of phospholipase C.
血清素(5-羟色胺,5-HT)刺激了与神经胶质细胞共培养的海马神经元中花生四烯酸的释放,但对单独培养的神经胶质细胞无此作用。5-HT刺激的肌醇磷酸释放也观察到了类似结果。这些结果表明这两种反应均起源于神经而非神经胶质细胞。药理学研究表明,花生四烯酸和肌醇磷酸的释放是由2型5-HT(5-HT2)受体介导的。在含有高水平5-HT2受体的皮质神经元中也检测到了5-HT刺激的花生四烯酸释放,但在5-HT2受体水平非常低或缺乏该受体的纹状体、脊髓或小脑颗粒细胞中未检测到。佛波酯12-肉豆蔻酸13-乙酸酯增强了5-HT刺激的花生四烯酸释放,但抑制了5-HT刺激的肌醇磷酸释放。5-HT刺激的花生四烯酸释放而非肌醇磷酸释放依赖于细胞外钙。5-HT刺激了[3H]胆碱标记细胞中[3H]溶血磷脂酰胆碱的释放,而[3H]胆碱或磷酸[3H]胆碱的释放没有增加。这些数据表明,5-HT通过激活磷脂酶A2刺激海马神经元中花生四烯酸的释放,与磷脂酶C的激活无关。