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

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.

Pubmed ID: 17558391


  • Chan CS
  • Guzman JN
  • Ilijic E
  • Mercer JN
  • Rick C
  • Tkatch T
  • Meredith GE
  • Surmeier DJ



Publication Data

June 28, 2007

Associated Grants


Mesh Terms

  • 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