Mechanisms of calcium influx following stroke

Abstract

Stroke is followed by a dramatic increase in intracellular calcium. This excessive increase in calcium levels is critical in the initiation of neuronal cell death. N-Methyl-D-aspartate (NMDA) receptor and L-type voltage-dependent calcium channel antagonists were unsuccessful at providing neuroprotection following ischemia in clinical trials. Therefore, recent research has focused on identifying novel mechanisms of calcium influx. This chapter reviews the evidence which links various receptors, channels, and transporters to calcium influx following stroke. Particular attention is paid to the therapeutic potential of targeting these various pathways.