Antiparkinsonian effect of flupirtine in monoamine-depleted rats |
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Authors: | M Schwarz M Nolden-Koch J Purr G Pergande F Block |
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Institution: | (1) Present address: Department of Neurology, Technical University, Aachen;(2) ASTA Medica Germany, Frankfurt, Federal Republic of Germany |
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Abstract: | Summary Excitatory amino acid receptor antagonists lead to marked suppression of parkinsonian-like symptoms in rodent and primate models of Parkinson's disease and are able to potentiate the ability of L-DOPA to reverse akinesia and ameliorate muscular rigidity displayed in these animal models. Flupirtine, which is clinically used as a non-opioid analgesic agent, has some N-methyl-D-aspartate (NMDA) antagonistic properties in several in vivo and in vitro experiments. We now report that in monoamine depleted rats (pretreated with reserpine, 5 mg/kg, and -methyl-para-tyrosine, 250mg/ kg i.p.) flupirtine dose-dependently (1–20mg/kg i.p.) suppressed rigidity, measured as tonic EMG activity in the gastrocnemius muscle, but had no effect on akinesia, measured as locomotor activity. In addition, it potentiated the antiparkinsonian effect of L-DOPA on akinesia and rigidity in this rodent model of Parkinson's disease. These effects of flupirtine are of particular clinical relevance, since flupirtine is devoid of the typical side effects of NMDA-receptor antagonists. |
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Keywords: | Locomotor activity EMG activity monoamine-depletion reserpine d-methyl-p-tyrosine L-DOPA flupirtine rats Parkinson's disease |
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