'Rejuvenation' protects neurons in mouse models of Parkinson's disease.
Journal:
Nature 2007 JunAuthors:
Chan CS, Guzman JN, Ilijic E, Mercer JN, Rick C, Tkatch T, Meredith GE, Surmeier DJ
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 pacema
...[more]king 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.[less]
Mesh Headings:
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Aging, Animals, Antiparkinson Agents, Calcium, Calcium Channels, L-Type, Dendrites, Disease Models, Animal, Disease Progression, Dopamine, Electric Conductivity, Gene Deletion, Male, Mice, Mice, Inbred C57BL, Mitochondria, Models, Neurological, Neurons, Parkinson Disease, Rotenone, Substantia Nigra