Dyck L E, Boulton A A
Department of Psychiatry, University of Saskatchewan, Saskatoon, Canada.
Neurochem Res. 1989 Jan;14(1):63-7. doi: 10.1007/BF00969759.
The effects of the trace amine, beta-phenylethylamine, on the hydrolysis of inositol phospholipids in rat cerebral cortical slices was studied using a direct assay involving prelabeling with [3H]inositol and then examining the production of [3H]inositol phosphates in the presence of lithium. Phenylethylamine exhibited two different effects. Millimolar concentrations of phenylethylamine stimulated the production of [3H]inositol phosphates to about 200% of control, while much smaller concentrations (micromolar) inhibited noradrenaline(NE)-stimulated [3H]inositol phosphate formation dose-dependently. The alpha 1-antagonist, prazosin, inhibited the increases in [3H]polyphosphoinositide turnover stimulated by phenylethylamine and by NE, though it inhibited phenylethylamine to a lesser extent than NE. It appears, therefore, that phenylethylamine affects [3H]inositol phosphate formation by acting as a partial alpha 1-agonist.
利用一种直接检测方法研究了痕量胺β-苯乙胺对大鼠大脑皮层切片中肌醇磷脂水解的影响,该方法包括先用[³H]肌醇进行预标记,然后在锂存在的情况下检测[³H]肌醇磷酸的生成。苯乙胺表现出两种不同的效应。毫摩尔浓度的苯乙胺可使[³H]肌醇磷酸的生成量刺激至对照的约200%,而浓度小得多(微摩尔)时则剂量依赖性地抑制去甲肾上腺素(NE)刺激的[³H]肌醇磷酸形成。α1拮抗剂哌唑嗪抑制了苯乙胺和NE刺激的[³H]多磷酸肌醇周转增加,不过它对苯乙胺的抑制程度小于对NE的抑制程度。因此,似乎苯乙胺通过作为部分α1激动剂来影响[³H]肌醇磷酸的形成。