Continued administration of GM1 ganglioside is required to maintain recovery from neuroleptic-induced sensorimotor deficits in MPTP-treated mice

doi:10.1016/0024-3205(89)90017-9

Life Sciences

Volume 45, Issue 25, 1989, Pages 2495-2502

https://doi.org/10.1016/0024-3205(89)90017-9 Get rights and content

Abstract

Injection of a dose of haloperidol that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and sensory neglect in MPTP- treated mice. Chronic GM1 ganglioside administration improves the behavioral impairments, partially restores striatal dopamine (DA) content and prevents DA D-2 receptor up-regulation. Discontinuation of GM1 ganglioside treatment results in a time-dependent decline of striatal DA content to pretreatment pathological levels, return of haloperidol-induced sensorimotor deficits and a rise of DA D-2 receptor density in the striatum. Apparently, continuous administration of GM1 ganglioside is necessary to maintain the biochemical and behavioral recovery in the MPTP-treated mouse. These observations may provide useful cues for understanding the mechanism of action of GM1 ganglioside.

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Continued administration of GM1 ganglioside is required to maintain recovery from neuroleptic-induced sensorimotor deficits in MPTP-treated mice

Abstract

Neuroscience

Dev. Brain Res.

Brain Res.

Brain Res.

Brain Res.

Neurosci. Lett.

Neurosci. Lett.

Brain Res.

Eur. J. Pharmacol.

Life Sci.

J. Biol. Chem.

Neurosci. Lett.