Abstract
Calcium subserves a ubiquitous role in the organisation of cell function. Ca2+ channels which control influx may be modified in disease states. Animal models of cerebral ischaemia do present some problems when investigating potential therapies involving Ca2+ channels. However, it is important not to be too rigid in searching for models which exactly mimic the human disease state, when even the best experimental approaches fall short of such an ideal. There are differences between different classes of calcium entry blocking drugs with regard to their activity on Ca2+ channels and transmembrane Ca2+ movement. Some calcium antagonists may also affect ion channels other than Ca2+, and this potential is exemplified by the novel ion channel modulator RS-87476, which affords experimental neurocytoprotection. Limitation of intracellular Na+ influx during ischaemia-induced depolarization may be useful.