JOURNAL ARTICLE

'Rejuvenation' protects neurons in mouse models of Parkinson's disease

C Savio Chan, Jaime N Guzman, Ema Ilijic, Jeff N Mercer, Caroline Rick, Tatiana Tkatch, Gloria E Meredith, D James Surmeier
Nature 2007 June 28, 447 (7148): 1081-6
17558391
Why dopamine-containing neurons of the brain's substantia nigra pars compacta die in Parkinson's disease has been an enduring mystery. Our studies suggest that the unusual reliance of these neurons on L-type Ca(v)1.3 Ca2+ channels to drive their maintained, rhythmic pacemaking renders them vulnerable to stressors thought to contribute to disease progression. The reliance on these channels increases with age, as juvenile dopamine-containing neurons in the substantia nigra pars compacta use pacemaking mechanisms common to neurons not affected in Parkinson's disease. These mechanisms remain latent in adulthood, and blocking Ca(v)1.3 Ca2+ channels in adult neurons induces a reversion to the juvenile form of pacemaking. Such blocking ('rejuvenation') protects these neurons in both in vitro and in vivo models of Parkinson's disease, pointing to a new strategy that could slow or stop the progression of the disease.

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