Martin L L, Neale R F, Wood P L
Pharmaceuticals Division, CIBA-GEIGY Corporation, Summit, NJ 07901.
Brain Res. 1987 Sep 1;419(1-2):239-43. doi: 10.1016/0006-8993(87)90589-0.
Chronic treatment with clorgyline, a type A monoamine oxidase (MAO) inhibitor (1 mg/kg/day for 11 days), reduced the number (Bmax) but not the affinity (Kd) of [3H]tryptamine binding sites in rat frontal/parietal cortical membranes. Binding was reduced for at least 36 days following the last injection. The reduction in [3H]tryptamine binding was dose-related and appeared to be maximal following a daily dose of 3 mg/kg. Chronic treatment with deprenyl, a type B MAO inhibitor (1 mg/kg/day for 11 days), did not affect [3H]tryptamine binding. Acute clorgyline administration (11 mg/kg) also had no effect. These data suggest that [3H]tryptamine binds to neurotransmitter receptors for tryptamine since mere chemical recognition sites would not be expected to be modulated by chronic drug treatment. Also, since [3H]tryptamine binding was down-regulated by a type A, but not a type B, MAO inhibitor, tryptamine may be selectively metabolized by type A MAO in vivo.
用A型单胺氧化酶（MAO）抑制剂氯吉兰进行慢性治疗（1毫克/千克/天，持续11天），可减少大鼠额叶/顶叶皮质膜中[3H]色胺结合位点的数量（Bmax），但不影响其亲和力（Kd）。末次注射后，结合减少至少36天。[3H]色胺结合的减少与剂量相关，每日剂量为3毫克/千克时似乎达到最大。用B型MAO抑制剂司来吉兰进行慢性治疗（1毫克/千克/天，持续11天），不影响[3H]色胺结合。急性给予氯吉兰（11毫克/千克）也无影响。这些数据表明，[3H]色胺与色胺的神经递质受体结合，因为单纯的化学识别位点预计不会受到慢性药物治疗的调节。此外，由于[3H]色胺结合可被A型而非B型MAO抑制剂下调，色胺在体内可能被A型MAO选择性代谢。
