Yoshiyama M, Roppolo J R, Rihmland J, Blastos B, de Groat W C
Department of Pharmacology, School of Medicine, University of Pittsburgh, PA 15261.
Neurosci Lett. 1991 May 27;126(2):141-4. doi: 10.1016/0304-3940(91)90539-6.
The effects of MK-801 (Dizocilpine) on the micturition reflex were studied in rats anesthetized with urethane (1.2 g/kg, s.c.). MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist (1-1000 micrograms/kg, i.v.) reduced, in a dose-dependent fashion the amplitude of rhythmic bladder contractions recorded isovolumetrically via a transurethral catheter. The largest doses (300-1000 micrograms/kg) completely abolished bladder activity. Bilateral section of the hypogastric nerves had no effect on MK-801 induced inhibition. MK-801 did not inhibit the bladder contractions induced by electrical stimulation of the pelvic nerve. These data suggest that MK-801 acts in the central nervous system to block glutaminergic excitatory transmission in the central micturition reflex pathway.
研究了MK-801(地佐环平)对用氨基甲酸乙酯(1.2 g/kg,皮下注射)麻醉的大鼠排尿反射的影响。MK-801是一种非竞争性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂(1-1000微克/千克,静脉注射),它以剂量依赖的方式降低了通过经尿道导管等容记录的节律性膀胱收缩的幅度。最大剂量(300-1000微克/千克)完全消除了膀胱活动。双侧切断腹下神经对MK-801诱导的抑制没有影响。MK-801不抑制电刺激盆神经诱导的膀胱收缩。这些数据表明,MK-801在中枢神经系统中起作用,阻断中枢排尿反射通路中的谷氨酰胺能兴奋性传递。