Maj J, Rogóz Z, Skuza G, Sowińska H
J Neural Transm. 1982;55(1):19-25. doi: 10.1007/BF01243338.
It has previously been found that a number of typical and atypical antidepressants, given chronically, intensify clonidine-induced aggressiveness in mice. Further experiments now show that chronic, but not acute, administration of nisoxetine, a selective inhibitor of noradrenaline uptake, potentiates clonidine-induced aggressiveness. Citalopram and fluvoxamine, two selective inhibitors of serotonin uptake, have no such action. Of the two isomers of flupenthixol, only the trans-form potentiates clonidine-induced aggressiveness of chronic experiments. The cis-form induces an inhibiting effect. Clonidine-induced aggressiveness is also intensified by chronic, but not by acute, administration of pizotifen, an antagonist fo serotonin and noradrenaline. The results seem to support the previous hypothesis that potentiation of clonidine-induced aggressiveness is mediated by an alpha 1-adrenergic mechanism.
此前已发现，多种典型和非典型抗抑郁药长期给药会增强可乐定诱导的小鼠攻击性。进一步的实验表明，去甲肾上腺素摄取的选择性抑制剂尼索西汀长期给药（而非急性给药）会增强可乐定诱导的攻击性。5-羟色胺摄取的两种选择性抑制剂西酞普兰和氟伏沙明则无此作用。氟哌噻吨的两种异构体中，只有反式异构体在慢性实验中会增强可乐定诱导的攻击性。顺式异构体则产生抑制作用。5-羟色胺和去甲肾上腺素拮抗剂匹莫齐特长期给药（而非急性给药）也会增强可乐定诱导的攻击性。这些结果似乎支持了之前的假设，即可乐定诱导的攻击性增强是由α1-肾上腺素能机制介导的。
