title: Redox regulation of neuronal voltage-gated calcium channels.
abstract: CONCLUSIONS
  Voltage-gated calcium channels are ubiquitously expressed in neurons and are key regulators of cellular excitability and synaptic transmitter release. There is accumulating evidence that multiple subtypes of voltage-gated calcium channels may be regulated by oxidation and reduction. However, the redox mechanisms involved in the regulation of channel function are not well understood.
  
  
  BACKGROUND
  Several studies have established that both T-type and high-voltage-activated subtypes of voltage-gated calcium channel can be redox-regulated. This article reviews different mechanisms that can be involved in redox regulation of calcium channel function and their implication in neuronal function, particularly in pain pathways and thalamic oscillation.
  
  
  RESULTS
  A current critical issue in the field is to decipher precise mechanisms of calcium channel modulation via redox reactions. In this review we discuss covalent post-translational modification via oxidation of cysteine molecules and chelation of trace metals, and reactions involving nitric oxide-related molecules and free radicals. Improved understanding of the roles of redox-based reactions in regulation of voltage-gated calcium channels may lead to improved understanding of novel redox mechanisms in physiological and pathological processes.
  
  
  CONCLUSIONS
  Identification of redox mechanisms and sites on voltage-gated calcium channel may allow development of novel and specific ion channel therapies for unmet medical needs. Thus, it may be possible to regulate the redox state of these channels in treatment of pathological process such as epilepsy and neuropathic pain.
authors.affiliation: 1 Department of Anesthesiology, University of Virginia School of Medicine , Charlottesville, Virginia.
authors.forename: Slobodan M
authors.initials: SM
authors.lastname: Todorovic
authors.forename: Vesna
authors.initials: V
authors.lastname: Jevtovic-Todorovic
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D020747:Calcium Channels, T-Type / Q000378:metabolism; D002384:Catalysis; D003545:Cysteine / Q000378:metabolism; D006801:Humans; D008670:Metals / Q000737:chemistry / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D020033:Protein Isoforms; D008063:Thioctic Acid / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D015220:Calcium Channels; D020747:Calcium Channels, T-Type; D008670:Metals; D020033:Protein Isoforms; D009569:Nitric Oxide; D008063:Thioctic Acid; D003545:Cysteine; D002118:Calcium