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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Veröffentlicht in:Pharmacology, biochemistry and behavior biochemistry and behavior, 2006-07, Vol.84 (3), p.415-419
Hauptverfasser: 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.
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Sprache:eng
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Zusammenfassung: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.
ISSN:0091-3057
1873-5177
DOI:10.1016/j.pbb.2006.05.027