Relationships Between ATP Sensitive Potassium Channels And Parkinson's Disease

Parkinson's disease (PD) is one of the most common neurodegenerative movement disorders, affecting approximately 2% of the population elder than 65 years old, the cardinal features of which include tremor, rigidity, slowness of movement and postural instability. The pathological hallmarks and biochemical changes of PD are the loss of nigrostriatal dopaminergic neurons, the reduction of dopamine (DA) content in the striatum and the presence of intraneuronal proteinacious cytoplasmic inclusions, termed "Lewy Bodies". Up till now, the underlying mechanisms for the loss of dopaminergic neurons remain unclear. Lines of evidence have revealed that the pathogenesis of cell death in PD is associated with excitotoxicity, energy defects, and oxidative damage processes. Therapeutic strategies derived from these, such as L-DOPA administration, are essentially symptomatical or accompanied with serious side effects, and cannot stop the progressive loss of dopaminergic neurons. Hence, many studies are focused on searching for new potential therapeutic targets and agents for the treatment of PD.In the past decade, some studies have focused on the pathophysiological role of K_ATP in PD. K_ATP are activated by a decrease in ATP/ADP ratio, coupling cell metabolism with its membrane potential. Functional K_ATP are heteroctameric complexs, consisting of four Kir6.x subunits and four regulatory SUR subunits. Currently, two main members...