Abstract
The neurotransmitter gamma-aminobuteric acid (GABA) is believed to have a controlling action on spinal locomotor networks. In spasticity, spinal locomotor networks are thought to play a role. A well known drug in the treatment of spasticity is the GABA(B) agonist Baclofen. We report an inhibitory effect of Baclofen on the ANP-mediated cGMP synthesis in the superficial dorsal horn (laminae I-III) of the rat cervical spinal cord. This inhibitory effect of Baclofen could not be detected after incubation with the NO donor SNP. The clinical effect of Baclofen on the reduction of spasticity might be explained by an enhancement of GABAergic inhibition of ANP mediated cGMP concentration in the spinal cord dorsal horn, thus reducing afferent input.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aging / metabolism
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Animals
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Atrial Natriuretic Factor / antagonists & inhibitors*
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Atrial Natriuretic Factor / metabolism
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Baclofen / pharmacology*
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Cervical Vertebrae
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Cyclic GMP / biosynthesis*
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GABA Agonists / pharmacology*
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GABA-B Receptor Agonists
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Immunohistochemistry
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Male
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Muscle Spasticity / drug therapy*
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Muscle Spasticity / metabolism
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Muscle Spasticity / physiopathology
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Nerve Net / drug effects
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Nerve Net / growth & development
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Nerve Net / metabolism
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Nitric Oxide Donors / pharmacology
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Nociceptors / drug effects
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Nociceptors / metabolism
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Pain / drug therapy
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Pain / metabolism
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Pain / physiopathology
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Posterior Horn Cells / drug effects*
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Posterior Horn Cells / growth & development
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Posterior Horn Cells / metabolism
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Rats
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Rats, Inbred Lew
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Receptors, GABA-B / metabolism*
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gamma-Aminobutyric Acid / metabolism*
Substances
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GABA Agonists
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GABA-B Receptor Agonists
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Nitric Oxide Donors
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Receptors, GABA-B
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gamma-Aminobutyric Acid
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Atrial Natriuretic Factor
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Cyclic GMP
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Baclofen