Calpains and delayed calcium deregulation in excitotoxicity.
Overactivation of glutamate receptors results in neurodegeneration in a variety of brain pathologies, including ischemia, epilepsy, traumatic brain injury and slow-progressing neurodegenerative disorders. In all these pathologies, it is well accepted that the calcium-dependent cysteine proteases calpains are key players in the mechanisms of neuronal cell death. Many research groups have been actively pursuing to establish a link between the deregulation of intracellular Ca(2+) homeostasis associated with excitotoxicity and calpain activity. It is well established that these two events are connected and interact synergistically to promote neurodegeneration, but whether calpain activity depends on or contributes to Ca(2+) deregulation is still under debate.
Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal. inaraujo@cnc.cj.uc.pt
Inês M
IM
Araújo
Bruno P
BP
Carreira
Caetana M
CM
Carvalho
Arsélio P
AP
Carvalho
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002154:Calpain / Q000378:metabolism / Q000502:physiology*; D004789:Enzyme Activation; D006706:Homeostasis; D006801:Humans; D017470:Receptors, Glutamate / Q000502:physiology*
D017470:Receptors, Glutamate; D002154:Calpain; D002118:Calcium