Title:The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative
Disorders
Volume: 21
Issue: 2
Author(s): Bernardo H.M. Correa, Carlos Roberto Moreira, Michael E. Hildebrand and Luciene Bruno Vieira*
Affiliation:
- Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas
Gerais, Brazil
Keywords:
Calcium channels, neurodegenerative disorders, parkinson’s disease, huntington’s disease, basal ganglia and cell death.
Abstract: Calcium (Ca2+) plays a central role in regulating many cellular processes and influences
cell survival. Several mechanisms can disrupt Ca2+ homeostasis to trigger cell death, including oxidative
stress, mitochondrial damage, excitotoxicity, neuroinflammation, autophagy, and apoptosis.
Voltage-gated Ca2+ channels (VGCCs) act as the main source of Ca2+ entry into electrically excitable
cells, such as neurons, and they are also expressed in glial cells such as astrocytes and oligodendrocytes.
The dysregulation of VGCC activity has been reported in both Parkinson's disease (PD)
and Huntington's (HD). PD and HD are progressive neurodegenerative disorders (NDs) of the basal
ganglia characterized by motor impairment as well as cognitive and psychiatric dysfunctions. This
review will examine the putative role of neuronal VGCCs in the pathogenesis and treatment of central
movement disorders, focusing on PD and HD. The link between basal ganglia disorders and
VGCC physiology will provide a framework for understanding the neurodegenerative processes that
occur in PD and HD, as well as a possible path towards identifying new therapeutic targets for the
treatment of these debilitating disorders.