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Substantia nigra: A site of action of muscle relaxant drugs
Author(s) -
Turski Lechoslaw,
Klockgether Thomas,
Schwarz Michael,
Turski Waldemar A.,
Sontag KarlHeinz
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410280307
Subject(s) - substantia nigra , muscle relaxant , baclofen , muscle tone , spasticity , medicine , pharmacology , apomorphine , tegmentum , dantrolene , dopaminergic , neuroscience , endocrinology , anesthesia , midbrain , agonist , dopamine , biology , receptor , central nervous system , calcium
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‐pro 2 ‐D‐phe 7 ‐D‐trp 9 ]‐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.