Parkinson's disease: return of an old prime suspect.

摘要

Pacemaking activity in adult substantia nigra (SN) dopamine neurons relies on L-type Ca(2+) channels, but a surprising study in Nature by Chan et al. demonstrates that blockade of these channels by dihydropyridines re-establishes the pacemaking driven by sodium and HCN channels found in juvenile SN. This shift protects SN neurons in chemical models of Parkinson's disease (PD), suggesting that elevated intracellular Ca(2+) participates in SN cell loss and that dihydropyridines may provide therapy in PD.