title: Calcium-permeable ion channels involved in glutamate receptor-independent ischemic brain injury.
abstract: Brain ischemia is a leading cause of death and long-term disabilities worldwide. Unfortunately, current treatment is limited to thrombolysis, which has limited success and a potential side effect of intracerebral hemorrhage. Searching for new cell injury mechanisms and therapeutic interventions has become a major challenge in the field. It has been recognized for many years that intracellular Ca(2+) overload in neurons is essential for neuronal injury associated with brain ischemia. However, the exact pathway(s) underlying the toxic Ca(2+) loading remained elusive. This review discusses the role of two Ca(2+)-permeable cation channels, TRPM7 and acid-sensing channels, in glutamate-independent Ca(2+) toxicity associated with brain ischemia.
authors.affiliation: Department of Psychology, Washington State University, Vancouver, WA, USA.
authors.forename: Ming-hua
authors.initials: MH
authors.lastname: Li
authors.forename: Koichi
authors.initials: K
authors.lastname: Inoue
authors.forename: Hong-fang
authors.initials: HF
authors.lastname: Si
authors.forename: Zhi-gang
authors.initials: ZG
authors.lastname: Xiong
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000378:metabolism*; D006801:Humans; D009474:Neurons / Q000378:metabolism; D010539:Permeability; D017346:Protein Serine-Threonine Kinases; D017470:Receptors, Glutamate / Q000378:metabolism*; D050053:TRPM Cation Channels / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
chemical_list: D017470:Receptors, Glutamate; D050053:TRPM Cation Channels; D017346:Protein Serine-Threonine Kinases; C486583:TRPM7 protein, human; D002118:Calcium