‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease

C. Savio Chan, Jaime N. Guzman, Ema Ilijic, Jeff N. Mercer, Caroline Rick, Tatiana Tkatch, Gloria E. Meredith and D. James Surmeier ()
Additional contact information
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
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

Nature, 2007, vol. 447, issue 7148, 1081-1086

Abstract: 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.

Date: 2007
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/nature05865 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:447:y:2007:i:7148:d:10.1038_nature05865

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature05865

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().