Abstract
AbstractDisturbance of Ca2+ homeostasis is assumed to precede ischemia‐induced neuronal death. Using the 4‐vessel occlusion model of cerebral ischemia and induction of ischemic tolerance in the rat, we studied the intracellular Ca2+ activated Ca2+ channel, the ryanodine receptor (RyR), by means of in situ hybridisation and immunohistochemistry. We found the level of RyR2 mRNA increased in CA1 and CA3 of the ischemic vulnerable hippocampus following 3 minutes of tolerance inducing ischemia, whereas 9 minutes of ischemia lead to an increased mRNA level in CA1 in contrast to a decrease in CA3. In ischemic tolerant animals (3 + 8.5 minutes of ischemia) the mRNA level was decreased in CA3. In all experimental groups, RyR1 mRNA remained unaltered, whereas RyR3 mRNA decreased in DG. Immunohistochemistry revealed no alterations of the RyR protein level in all the ischemic groups compared to sham‐operated animals. Taken together, these changes do not clarify if the RyR is involved in tolerance induction or in the degenerative process leading to ischemic delayed neuronal death.
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