A complex interaction of environmental, genetic and epigenetic factors combine with ageing to cause the most prevalent of movement disorders Parkinson's disease. Current pharmacological treatments only tackle the symptoms and do not stop progression of the disease or reverse the neurodegenerative process. While some incidences of Parkinson's disease arise through heritable genetic defects, the cause of the majority of cases remains unknown. Likewise, why some neuronal populations are more susceptible to neurodegeneration than others is not clear, but as the molecular pathways responsible for the process of cell death are unravelled, it is increasingly apparent that disrupted cellular energy metabolism plays a central role. Precise control of cellular calcium concentrations is crucial for maintenance of energy homeostasis. Recently, differential cellular expression of neuronal voltage-gated calcium channel (Ca(V)) isoforms has been implicated in the susceptibility of vulnerable neurons to neurodegeneration in Parkinson's disease. Ca(V) channels are also involved in the synaptic plasticity response to the denervation that occurs in Parkinson's disease and following chronic treatment with anti-parkinsonian drugs. This review will examine the putative role neuronal Ca(V) channels have in the pathogenesis and treatment of Parkinson's disease.
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