Voltage-Gated Calcium Channel Blockers for the Treatment of Traumatic Brain Injury

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations

Abstract

Traumatic brain injury (TBI) is a leading cause of death and disability in the United States, and, to date, no pharmacological agents are known to improve neurological outcome following injury. TBI is associated with a severity-dependent accumulation of intracellular calcium ([Ca2+]i) lasting hours-to-days postinjury and driving apoptotic and necrotic cell death. Pathological accumulation of calcium can also lead to breakdown of structural proteins and changes in gene expression resulting in long-term dysfunction of surviving cells. In in vitro models of TBI, L- and N-type voltage-gated calcium channel (VGCC) blockers reduced [Ca2+]i accumulation and glutamate release resulting in reduced cell death. In rodent models of TBI, administration of VGCC blockers reduced cell death and improved spatial learning and motor function. Based on these data, there is a clear role of VGCC in postinjury pathophysiology, and manipulation of these channels has the potential to improve neurological outcome following injury.

Original languageEnglish (US)
Title of host publicationNew Therapeutics for Traumatic Brain Injury
Subtitle of host publicationPrevention of Secondary Brain Damage and Enhancement of Repair and Regeneration
PublisherElsevier Inc.
Pages179-197
Number of pages19
ISBN (Electronic)9780128027011
ISBN (Print)9780128026861
DOIs
StatePublished - Oct 17 2016

Keywords

  • Antagonists
  • Cognition
  • Neuroprotection
  • Small peptide antagonists
  • Traumatic brain injury
  • Voltage-gated calcium channels

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

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  • Cite this

    Gurkoff, G. G., Shahlaie, K., Lyeth, B. G., & Berman, R. F. (2016). Voltage-Gated Calcium Channel Blockers for the Treatment of Traumatic Brain Injury. In New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration (pp. 179-197). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-802686-1.00011-0