Wüllner U, Klockgether T, Sontag K H
Max-Planck-Institute for Experimental Medicine, Göttingen, F.R.G.
Brain Res. 1989 Sep 4;496(1-2):341-4. doi: 10.1016/0006-8993(89)91085-8.
The action of phaclofen, the phosphonic acid derivative of baclofen, on baclofen-induced suppression of spinal reflex transmission was tested in anaesthetized rats. Intrathecal (i.th.) injection of phaclofen, 100 nmol, antagonized the depressant effect of baclofen, 2 nmol, on spinal Hoffmann (H)-reflexes and polysynaptic flexor reflexes but ha on the action of muscimol, 20 nmol. The antagonistic effect of phaclofen on baclofen-induced depression of H-reflexes was dose-dependent in doses ranging from 1 to 100 nmol. When administered alone, phaclofen, 100 nmol, was devoid of stimulatory or depressant effects on spinal reflexes. These results indicate that phaclofen specifically antagonizes the reflex suppressant action of baclofen. The lack of intrinsic action of phaclofen suggests that there is no endogenous tonic inhibition mediated by GABAB receptors under the present experimental conditions.
在麻醉大鼠中测试了巴氯芬的膦酸衍生物法氯芬对巴氯芬诱导的脊髓反射传递抑制的作用。鞘内注射100纳摩尔法氯芬可拮抗2纳摩尔巴氯芬对脊髓霍夫曼(H)反射和多突触屈肌反射的抑制作用,但对20纳摩尔蝇蕈醇的作用无影响。法氯芬对巴氯芬诱导的H反射抑制的拮抗作用在1至100纳摩尔的剂量范围内呈剂量依赖性。单独给药时,100纳摩尔法氯芬对脊髓反射无刺激或抑制作用。这些结果表明法氯芬特异性拮抗巴氯芬的反射抑制作用。法氯芬缺乏内在作用表明在当前实验条件下不存在由GABAB受体介导的内源性强直抑制。