| First Author | Chan CS | Year | 2007 |
| Journal | Nature | Volume | 447 |
| Issue | 7148 | Pages | 1081-6 |
| PubMed ID | 17558391 | Mgi Jnum | J:122762 |
| Mgi Id | MGI:3715410 | Doi | 10.1038/nature05865 |
| Citation | Chan CS, et al. (2007) 'Rejuvenation' protects neurons in mouse models of Parkinson's disease. Nature 447(7148):1081-6 |
| abstractText | 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. |
