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- W2069030534 abstract "NMDA-mediated neurotoxicity and oxidative stress have been implicated in the etiology of a number of degenerative diseases including motor neuron disease. The present study examined the effect of chronic administration of the glycine/NMDA receptor antagonist L-701,324 and the monoamine oxidase B inhibitor (r)-deprenyl on the onset and rate of progression of neurological impairment in the motor neuron degeneration (mnd) mouse, a murine model of neurodegeneration. Neurological assessment ofmndmice revealed an onset of motor deficits at 6 months of age as observed by the loss of hindlimb reflex extension. By 7 months, balance was also markedly impaired as measured by deficits in rotarod performance and ability to remain on balancing beams. At 8 months of agemndmice exhibited gross abnormalities in walking pattern; animals were unable to flex their hindlimbs and tended to walk in small labored movements. Daily administration of L-701,324 (10 mg/kg p.o.) orr(−)-deprenyl (1 mg/kg p.o.) tomndmice from 4 to 8 months of age failed to delay the onset of symptoms or slow the rate of deterioration of motor performance. These findings suggest that excessive activation of NMDA receptors may not be involved in the pathological process leading to motor neuron dysfunction inmndmice and do not suggest a protective effect of deprenyl on motor neurons in these mice." @default.
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- W2069030534 date "1999-01-01" @default.
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- W2069030534 title "Onset and Progression of Motor Deficits in Motor Neuron Degeneration (mnd) Mice Are Unaltered by the Glycine/NMDA Receptor Antagonist L-701,324 or the MAO-B Inhibitorr(−)-Deprenyl" @default.
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- W2069030534 doi "https://doi.org/10.1006/exnr.1998.6873" @default.
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