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Inflammation plays a central role in stroke-induced brain injury. The alpha7 nicotinic acetylcholine receptor (a7nAChR) can modulate immune responses in both the periphery and the brain. The aims of the present study were to investigate a7nAChR expression in different brain regions and evaluate the potential effect of the selective a7nAChR agonist AR-R17779 on ischemia-reperfusion brain injury inmice. Droplet digital PCR (ddPCR) was used to evaluate the absolute expression of the gene encoding a7nAChR (Chrna7) in hippocampus, striatum, thalamus and cortex in adult, naïve mice. Mice subjected to transient middle cerebral artery occlusion (tMCAO) or sham surgery were treated with a7nAChR agonist AR-R17779 (12 mg/kg) or saline once daily for 5 days. Infarct size and microglial activation 7 days after tMCAO were analyzed using immunohistochemistry. Chrna7 expression was found in all analyzed brain regions in naïve mice with the highest expression in cortex and hippocampus. At sacrifice, white blood cell count was significantly decreased in AR-R17779 treated mice compared with saline controls in the sham groups, although, no effect was seen in the tMCAO groups. Brain injury and microglial activation were evident 7 days after tMCAO. However, no difference was found between mice treated with saline or AR-R17779. In conclusion, a7nAChR expression varies in different brain regions and, despite a decrease in white blood cells in sham mice receiving AR-R17779, this compound does not affect stroke-induced brain injury. [ABSTRACT FROM AUTHOR]