The importance of voltage-dependent sodium channels in cerebral ischaemia.
Strategies for the treatment of thromboembolic stroke are based on restoring the blood flow as soon as possible and protecting the neurons from the deleterious consequences of cerebral ischaemia. Interest has focused on blockers of voltage-dependent Na+ channels as potential neuroprotective agents because they prevent neuronal death in various experimental models of cerebral ischaemia and act cytoprotectively in models of white matter damage. Although several Na+ blockers are currently being tested in various phases of clinical development, most of these agents are relatively weak and unspecific. I therefore consider it worthwhile to search for molecules which specifically block voltage-dependent Na+ channels for the treatment of cerebral ischaemia.
Carter
A J
AJ
Department of Central Nervous System Research, Ingelheim am Rhein, Federal Republic of Germany.
D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D015640:Ion Channel Gating; D018696:Neuroprotective Agents / Q000627:therapeutic use; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology; D015424:Reperfusion; D015222:Sodium Channels / Q000502:physiology*
D018696:Neuroprotective Agents; D016194:Receptors, N-Methyl-D-Aspartate; D015222:Sodium Channels