Conn P J, Sanders-Bush E
J Pharmacol Exp Ther. 1985 Jul;234(1):195-203.
In rat cerebral cortex, serotonin (5-HT) stimulates phosphoinositide turnover with an EC50 of 1 microM in the presence of pargyline. The EC50 is 16-fold higher in the absence of pargyline. Selective S2 antagonists inhibit 5-HT-stimulated phosphoinositide turnover. Schild analysis of the blockade by ketanserin of the 5-HT effect gives an estimated Kd of ketanserin for the phosphoinositide-linked receptor of 11.7 nM, which agrees with the Kd (3.5 nM) of [3H]ketanserin for the S2 site. Furthermore, MK-212, 5-HT and 5-fluorotryptamine stimulate phosphoinositide turnover with potencies that resemble their potencies at the S2 but not the S1 binding site. Of 11 agonists tested, the tryptamine derivatives tend to be more efficacious than the piperazine derivatives. The selective S1 agonist 8-hydroxy-2-(di-N-propylamino)tetralin is inactive at stimulating phosphoinositide turnover. No significant relationship exists between the regional distributions of 5-HT-stimulated phosphoinositide turnover and S2 binding sites. Furthermore, the S2 antagonist ketanserin is less potent and less efficacious in hippocampus and limbic forebrain than in cerebral cortex. These data suggest that 5-HT-stimulated phosphoinositide turnover is linked to the S2 binding site in rat cerebral cortex. However, 5-HT increases phosphoinositide turnover in subcortical regions by mechanisms other than stimulation of the S2 receptor.
在大鼠大脑皮层中，在存在帕吉林的情况下，血清素（5-羟色胺，5-HT）刺激磷酸肌醇代谢，其半数有效浓度（EC50）为1微摩尔。在不存在帕吉林时，EC50高16倍。选择性S2拮抗剂抑制5-HT刺激的磷酸肌醇代谢。对酮色林阻断5-HT效应进行的希尔德分析得出，酮色林对磷酸肌醇连接受体的估计解离常数（Kd）为11.7纳摩尔，这与[3H]酮色林对S2位点的Kd（3.5纳摩尔）相符。此外，MK-212、5-HT和5-氟色胺刺激磷酸肌醇代谢的效能类似于它们在S2而非S1结合位点的效能。在所测试的11种激动剂中，色胺衍生物往往比哌嗪衍生物更有效。选择性S1激动剂8-羟基-2-（二-N-丙基氨基）四氢萘在刺激磷酸肌醇代谢方面无活性。5-HT刺激的磷酸肌醇代谢的区域分布与S2结合位点之间不存在显著关系。此外，S2拮抗剂酮色林在海马体和边缘前脑的效力和效能低于在大脑皮层的效力和效能。这些数据表明，5-HT刺激的磷酸肌醇代谢与大鼠大脑皮层中的S2结合位点相关。然而，5-HT通过刺激S2受体以外的机制增加皮层下区域的磷酸肌醇代谢。
