Author
Listed:
- C. Savio Chan
(Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA)
- Jaime N. Guzman
(Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA)
- Ema Ilijic
(Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA)
- Jeff N. Mercer
(Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA)
- Caroline Rick
(Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
Present address: BCTU, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.)
- Tatiana Tkatch
(Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA)
- Gloria E. Meredith
(Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, Chicago, Illinois 60064, USA)
- D. James Surmeier
(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 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.
Suggested Citation
C. Savio Chan & Jaime N. Guzman & Ema Ilijic & Jeff N. Mercer & Caroline Rick & Tatiana Tkatch & Gloria E. Meredith & D. James Surmeier, 2007.
"‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease,"
Nature, Nature, vol. 447(7148), pages 1081-1086, June.
Handle:
RePEc:nat:nature:v:447:y:2007:i:7148:d:10.1038_nature05865
DOI: 10.1038/nature05865
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