Dramatic and rapidly reversible structural changes are observed in dendritic spine morphology following excitotoxic or hypoxic stress1. However, morphological and biochemical alterations in post-synaptic densities persist for up to 24 hours following transient ischemia. This suggests that the synapse may be the origin of signals that propagate toward the cell body and instigate delayed post-ischemic neuronal death. Synaptically localized cell adhesion molecules are important regulators of synaptic plasticity and synaptogenesis. Regulation of cell adhesion and cytoskeletal structure in dendritic spines is necessary for the maintenance of mature synaptic connections. Therefore, we examined the effects of transient cerebral ischemia on the expression of synaptic proteins 20 hours post-ischemia.
Journal of Cerebral Blood Flow and Metabolism25 (2005): S219–.