Non-NMDAR neuronal Ca2+-permeable channels in delayed neuronal death and as potential therapeutic targets for ischemic brain damage

摘要

Introduction: Transient cerebral ischemia represents the most common cause of complex chronic disability in adults due to delayed neuronal death as a result of aberrant post-ischemic increases in the [Ca2+](c) and [Zn2+](c). A number of Ca2+-permeable channels are engaged in transient ischemia-induced neuronal death.