Previous studies suggest that the brain is capable of adapting to the brain injury due to ischemia, and that synaptic remodeling is important in this process. However, its biological mechanisms are not well understood. Arcadlin, a member of protocadherins, is involved in the synaptic plasticity, and Arcadlin Knockout increases the dendritic spine density in vitro. These notions imply the contribution of Arcadlin in the remodeling of neural network within the surviving tissue during the recovery from brain ischemia. In this study, we investigated the time course and the region of Arcadlin expression after cerebral ischemia. To induce permanent cerebral ischemia, C.B-17/Icr-+/+ Jcl wild-type male mice aged 7 weeks were subjected to middle cerebral artery occlusion (MCAO). Western blot analysis showed that Arcadlin is upregulated in hippocampus within 6 hours after MCAO. Sham operation did not induce the upregulation of Acadlin. We would like to discuss about the possible involvement of Arcadlin during the pathophysiological processes after the cerebral ischemia.