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Nature. 2007 Jun 28;447(7148):1081-6. Epub 2007 Jun 10.

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

Author information

1
Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.

Abstract

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.

PMID:
17558391
DOI:
10.1038/nature05865
[Indexed for MEDLINE]

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