Hyttel J
Acta Pharmacol Toxicol (Copenh). 1977 Mar;40(3):439-46.
Changes in endogenous concentrations of 5-HT and 5-HIAA as well as the turnover rate of 5-HT was studied in rat brain after treatment with a new potent and selective inhibitor of the neuronal 5-HT reuptake mechanism, Lu 10-171(1-(3-dimethylamino)propyl)-1-(p-fluorophenyl)-5-phthalancarbonitrile). After a single dose of Lu 10-171 the concentration of 5-HIAA was reduced from 1 to 24 hours after treatment, whereas that of 5-HT was practically unchanged, indicating decreased turnover of 5-HT in the brain. This was confirmed using three different methods for measuring 5-HT turnover. Thus the rate of 5-HIAA accumulation in the brain after probenecid was reduced after Lu 10-171. Likewise treatment with Lu 10-171 led to a decreased fall in 5-HT and an increased fall in 5-HIAA after inhibition of 5-HT synthesis with parachlorophenylalanine (PCPA). Unexpectedly Lu 10-171 did not change either the accumulation of 5-HT or the decrease in 5-HIAA after inhibition of MAO with pargyline. By and large the results are consistent with the proposed negative feed-back regulation of 5-HT neuronal firing rate due to the abundance of 5-HT at postsynaptic receptors after inhibition of the reuptake mechanism.
在用一种新型强效且选择性的神经元5-羟色胺(5-HT)再摄取机制抑制剂Lu 10-171(1-(3-二甲氨基)丙基)-1-(对氟苯基)-5-邻苯二甲腈)处理大鼠脑之后,研究了内源性5-HT和5-羟吲哚乙酸(5-HIAA)浓度的变化以及5-HT的周转率。单次给予Lu 10-171后,处理后1至24小时5-HIAA的浓度降低,而5-HT的浓度实际上未改变,这表明脑中5-HT的周转率降低。使用三种不同的方法测量5-HT周转率证实了这一点。因此,丙磺舒处理后脑中5-HIAA的积累速率在给予Lu 10-171后降低。同样,在用对氯苯丙氨酸(PCPA)抑制5-HT合成后,给予Lu 10-171导致5-HT的下降减少而5-HIAA的下降增加。出乎意料的是,在用优降宁抑制单胺氧化酶(MAO)后,Lu 10-171既未改变5-HT的积累也未改变5-HIAA的下降。总体而言,这些结果与以下观点一致:由于再摄取机制受到抑制后突触后受体处5-HT含量丰富,从而对5-HT神经元放电率存在负反馈调节。