Neuroprotective effects of caffeine in the model of 6-hydroxydopamine lesion in rats

The work shows the effects of caffeine after the intrastriatal injection of 6-OHDA in rats, considered as a model of Parkinson disease (PD). Two weeks after the 6-OHDA lesion, rats exhibit a characteristic rotation behavior as a response to the apomorphine challenge. Our results showed significant i...

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Published inPharmacology, biochemistry and behavior Vol. 84; no. 3; pp. 415 - 419
Main Authors Aguiar, Lissiana Magna Vasconcelos, Nobre, Hélio V., Macêdo, Danielle S., Oliveira, Aline A., Freitas, Rivelilson M., Vasconcelos, Silvânia M., Cunha, Geanne M.A., Sousa, Francisca Cléa F., Viana, Glauce Socorro B.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.07.2006
Elsevier Science
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Summary:The work shows the effects of caffeine after the intrastriatal injection of 6-OHDA in rats, considered as a model of Parkinson disease (PD). Two weeks after the 6-OHDA lesion, rats exhibit a characteristic rotation behavior as a response to the apomorphine challenge. Our results showed significant increases in the number of apomorphine-induced rotations in 6-OHDA-lesioned rats, as compared to sham-operated animals. A partial recovery was observed in 6-OHDA-lesioned rats, after caffeine (10 and 20 mg/kg, i.p., daily for 14 days) treatment. The stereotaxic injection of 6-OHDA produced loss of striatal neurons, as indicated by the decrease in monoamines levels, in the ipsilateral side (75–85%) when compared to the contralateral side. Significant decreases in noradrenaline levels were seen in the ipsilateral side of 6-OHDA group (62%), and this effect was not significantly reversed in caffeine-treated groups. While significant decreases in dopamine levels were seen in the ipsilateral side of 6-OHDA group (78%), in the caffeine-treated group (10 and 20 mg/kg, i.p.) the decreases were only 53 and 18%, indicating significant recoveries. In conclusion, our data demonstrated beneficial effects of caffeine in this model of PD, suggesting the potential use of A2A antagonists as a novel treatment for this neurodegenerative disease.
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ISSN:0091-3057
1873-5177
DOI:10.1016/j.pbb.2006.05.027