Turski L, Klockgether T, Schwarz M, Turski W A, Sontag K H
Max-Planck-Institute for Experimental Medicine, Göttingen, Federal Republic of Germany.
Ann Neurol. 1990 Sep;28(3):341-8. doi: 10.1002/ana.410280307.
Sites of action of centrally active muscle relaxant drugs are not well defined. Clinical experience with such drugs suggests that the spinal cord may be one of the important regions from which pathologically increased muscle tone may be relieved. Supraspinal centers that may also be involved in the expression of muscle relaxant action have not yet been defined. We report here that microinjections of therapeutically relevant muscle relaxants into the midbrain tegmentum of genetically spastic rats decrease muscle tone. The substantia nigra is the region from which midazolam, baclofen, and tizanidine (drugs used clinically in the treatment of spasticity), or gamma-vinyl-GABA, (-)-2-amino-7-phosphonoheptanoate, and [D-pro2-D-phe7-D-trp9]-substance P (experimental drugs active in animal models of spasticity), reduce muscle tone in genetically spastic rats and Hoffmann reflexes in normal rats. The effects of muscle relaxant drugs are topographically restricted to the substantia nigra pars reticulata and are receptor specific. These observations disclose a previously unknown function of the substantia nigra in mediating muscle relaxation.
中枢性肌肉松弛药物的作用部位尚未明确界定。此类药物的临床经验表明，脊髓可能是可缓解病理性肌张力增高的重要部位之一。可能也参与肌肉松弛作用表达的脊髓以上中枢尚未明确。我们在此报告，向遗传性痉挛大鼠的中脑被盖微量注射具有治疗相关性的肌肉松弛剂可降低肌张力。黑质是咪达唑仑、巴氯芬和替扎尼定（临床上用于治疗痉挛的药物）或γ-乙烯基-GABA、（-）-2-氨基-7-膦酰庚酸以及[D-脯氨酸2-D-苯丙氨酸7-D-色氨酸9]-P物质（在痉挛动物模型中具有活性的实验性药物）可降低遗传性痉挛大鼠肌张力并减弱正常大鼠霍夫曼反射的区域。肌肉松弛药物的作用在地形学上局限于黑质网状部，且具有受体特异性。这些观察结果揭示了黑质在介导肌肉松弛方面此前未知的功能。
