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Noradrenaline, an important transmitter in the CNS, is involved in cerebral plasticity and functional recovery after injury. Experimental brain injury, including KCl application onto the brain surface, induces a slow-moving cortical depolarization/depression wave called cortical spreading depression (CSD). Interestingly, CSD does not produce neuronal damage but can protect cortical neurons against subsequent neurotoxic insults, although the mechanisms involved are unknown. This study examined the status of alpha- and beta-adrenoceptors (ARs) in cerebral cortex following CSD. Anesthetized rats had unilateral CSD induced by a 10-min topical application of KCl to the frontoparietal cortex and were killed at various times thereafter. Levels of alpha1-, alpha2-, beta1-, and beta2-AR mRNA and binding were examined using in situ hybridization histochemistry and radioligand autoradiography. Levels of alpha1b-AR mRNA in the affected neocortex were significantly increased by 20-40% at 1, 2, and 7 days (P |
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