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

Oleh:

Chan, C. Savio ; Guzman, Jaime N. ; Ilijic, Ema ; Mercer, Jeff N. ; Rick, Caroline ; Tkatch, Tatiana ; Meredith, Gloria E. ; Surmeier, D. James

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: NATURE (keterangan: ada di Proquest) vol. 447 no. 7148 (Jun. 2007), page 1081.

Ketersediaan

Perpustakaan FK Nomor Panggil: N01.K.2007.06 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

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.

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