'Rejuvenation' protects neurons in mouse models of Parkinson's disease |
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Authors: | Chan C Savio Guzman Jaime N Ilijic Ema Mercer Jeff N Rick Caroline Tkatch Tatiana Meredith Gloria E Surmeier D James |
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Affiliation: | Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. |
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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. |
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