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ACS Chem Neurosci. 2012 Jan 18;3(1):22-30. doi: 10.1021/cn200072h. Epub 2011 Oct 26.

Ceftriaxone ameliorates motor deficits and protects dopaminergic neurons in 6-hydroxydopamine-lesioned rats.

Author information

1
Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong.

Abstract

Parkinson's disease is caused by the degeneration of dopaminergic neurons in substantia nigra. There is no current promising treatment for neuroprotection of dopaminergic neurons. Ceftriaxone is a beta-lactam antibiotic and has been reported to offer neuroprotective effects (Rothstein, J.-D., Patel, S., Regan, M.-R., Haenggeli, C., Huang, Y.-H., Bergles, D.-E., Jin, L., Dykes, H.-M., Vidensky, S., Chung, D.-S., Toan, S.-V., Bruijn, L.-I., Su, Z.-Z., Gupta, P., and Fisher, P.-B. (2005) Beta-lactam antibiotics offer neuroprotection by increasing glutamate transporter expression Nature433, 73-77). In the present study, efficacy of ceftriaxone in neuroprotection of dopaminergic neurons and amelioration of motor deficits in a rat model of Parkinson's disease were investigated. Ceftriaxone was administrated in 6-hydroxydopamine-lesioned rats. Using behavioral tests, grip strength and numbers of apomorphine-induced contralateral rotation were declined in the ceftriaxone-treated group. More importantly, cell death of dopaminergic neurons was found to decrease. In addition, both the protein expression and immunoreactivity for GLT-1 were up-regulated. The present results strongly indicate that ceftriaxone is a potential agent in the treatment of Parkinson's disease.

KEYWORDS:

Animal model of Parkinson’s disease; antibiotic; basal ganglia; ceftriaxone; degeneration of dopaminergic neurons; glutamate transporter; glutamate transporter subtype 1

PMID:
22860178
PMCID:
PMC3369786
DOI:
10.1021/cn200072h
[Indexed for MEDLINE]
Free PMC Article

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