Severson J A, Anderson B
J Neurosci Res. 1986;16(2):429-38. doi: 10.1002/jnr.490160210.
Chronic pretreatment of mice with the monoamine oxidase type B inhibitor (-)deprenyl resulted in an increase in the density of cerebral cortical 3H-imipramine binding sites and a decrease in the density of cerebral cortical beta-adrenergic receptors. In contrast, pretreatment of mice with the tricyclic antidepressants imipramine and desipramine did not alter the density of cerebral cortical 3H-imipramine binding sites. Imipramine and desipramine treatment decreased the density of beta-adrenergic receptors. Haloperidol pretreatment resulted in an increase in the density of striatal D-2 dopamine receptors, but did not alter the density of cerebral cortical 3H-imipramine binding sites or beta-adrenergic receptors. These data suggest that brain 3H-imipramine binding sites can be regulated by pharmacological pretreatment, but that this regulation may not occur for all antidepressants.
用单胺氧化酶B型抑制剂（-）司来吉兰对小鼠进行长期预处理，导致大脑皮质3H-丙咪嗪结合位点密度增加，大脑皮质β-肾上腺素能受体密度降低。相比之下，用三环类抗抑郁药丙咪嗪和地昔帕明对小鼠进行预处理，并未改变大脑皮质3H-丙咪嗪结合位点的密度。丙咪嗪和地昔帕明治疗降低了β-肾上腺素能受体的密度。氟哌啶醇预处理导致纹状体D-2多巴胺受体密度增加，但未改变大脑皮质3H-丙咪嗪结合位点或β-肾上腺素能受体的密度。这些数据表明，脑内3H-丙咪嗪结合位点可通过药物预处理进行调节，但并非所有抗抑郁药都会出现这种调节。
