Klimek V, Zak-Knapik J, Mackowiak M
Institute of Pharmacology, Polish Academy of Sciences, Kraków.
J Psychiatry Neurosci. 1994 Jan;19(1):63-7.
Repeated treatment with fluoxetine and citalopram, which are potent 5-HT reuptake inhibitors, resulted in different regulation of 5-HT1A and 5-HT2 receptors in the rat brain. Their effects were compared with those of other antidepressants: imipramine, mianserin and levoprotiline. The density of 5-HT1A receptors, labelled with [3H]8-OH-DPAT, in the rat hippocampus was enhanced after citalopram, imipramine, mianserin and levoprotiline, but not altered after fluoxetine administration. [3H]Ketanserin binding sites, which label 5-HT2 receptors, were increased after fluoxetine and levoprotiline, but decreased after citalopram, imipramine and mianserin in the rat cerebral cortex. Acute administration of fluoxetine, but not citalopram, resulted in a decreased density of 5-HT1A receptors. 5-HT2 receptors were not changed by acute administration of either fluoxetine or citalopram. The obtained results indicate that besides 5-HT reuptake inhibiting properties of both compounds, there may exist an additional mechanism(s) of their action, which leads to different regulation of 5-HT1A and 5-HT2 receptors.
强效5-羟色胺（5-HT）再摄取抑制剂氟西汀和西酞普兰的反复治疗导致大鼠脑中5-HT1A和5-HT2受体的不同调节。将它们的作用与其他抗抑郁药进行了比较：丙咪嗪、米安色林和左洛替林。用[3H]8-羟基二丙胺基四氢萘（[3H]8-OH-DPAT）标记的大鼠海马中5-HT1A受体的密度在给予西酞普兰、丙咪嗪、米安色林和左洛替林后增加，但在给予氟西汀后未改变。标记5-HT2受体的[3H]酮色林结合位点在给予氟西汀和左洛替林后增加，但在给予西酞普兰、丙咪嗪和米安色林后在大鼠大脑皮层中减少。急性给予氟西汀而非西酞普兰导致5-HT1A受体密度降低。急性给予氟西汀或西酞普兰均未改变5-HT2受体。所得结果表明，除了两种化合物的5-HT再摄取抑制特性外，它们可能还存在其他作用机制，导致5-HT1A和5-HT2受体的不同调节。
