Bouthillier A, de Montigny C
Neurosci Lett. 1987 Jan 27;73(3):271-5. doi: 10.1016/0304-3940(87)90257-6.
Long-term administration of various types of antidepressant drugs has been recently reported to reduce the density of benzodiazepine receptors in the rat CNS. In the present study, using the microiontophoretic technique, the effect of flurazepam application on cholecystokinin-induced activation of hippocampal pyramidal neurons was assessed in rats treated with the antidepressants desipramine, trimipramine and citalopram, and the antipsychotic chlorpromazine, for 3 weeks. All 3 antidepressant drugs, but not chlorpromazine, reduced the efficacy of flurazepam. A two-week treatment with desipramine produced a similar effect, whereas a one-week treatment with this drug failed to alter the effect of flurazepam. These results constitute further evidence that long-term antidepressant treatment down-regulates benzodiazepine receptors.
最近有报道称，长期服用各类抗抑郁药物会降低大鼠中枢神经系统中苯二氮䓬受体的密度。在本研究中，采用微离子电泳技术，评估了氟西泮对经抗抑郁药地昔帕明、曲米帕明和西酞普兰以及抗精神病药氯丙嗪治疗3周的大鼠胆囊收缩素诱导的海马锥体神经元激活的影响。所有3种抗抑郁药物（而非氯丙嗪）均降低了氟西泮的效力。地昔帕明两周的治疗产生了类似效果，而该药一周的治疗未能改变氟西泮的作用。这些结果进一步证明长期抗抑郁治疗会下调苯二氮䓬受体。
