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

CS Chan, JN Guzman, E Ilijic, JN Mercer, C Rick… - Nature, 2007 - nature.com
CS Chan, JN Guzman, E Ilijic, JN Mercer, C Rick, T Tkatch, GE Meredith, DJ Surmeier
Nature, 2007nature.com
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 Cav1. 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 …
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 Cav1.3 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 Cav1.3 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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