RT Journal Article SR Electronic T1 Developing of focal ischemia in the hippocampus or the amygdala reveals a regional compensation rule for fear memory acquisition JF eneuro JO eNeuro FD Society for Neuroscience SP ENEURO.0398-20.2021 DO 10.1523/ENEURO.0398-20.2021 A1 Cheng-Long Yu A1 Jin-Nan Li A1 Ping Gan A1 Li-Ping Wang A1 Yue-Xiong Yang A1 Da-Fu Yu A1 Rong-Rong Mao A1 Fu-Qiang Xu A1 Qi-Xin Zhou A1 Gal Richter-Levin A1 Lin Xu A1 Heng Zhou YR 2021 UL http://www.eneuro.org/content/early/2021/03/27/ENEURO.0398-20.2021.abstract AB Circuit compensation is often observed in patients with acute ischemic stroke, suggesting the importance of the interaction between brain regions. Also, contextual fear memory is an association between multisensory contexts and fearful stimuli, for which the interaction between the hippocampus and the amygdala is believed to be critical. To understand how focal ischemia in one region could influence the other region, we used a modified photo-thrombosis to induce focal ischemia in the hippocampus or the amygdala or both in freely-moving rats. We found that the learning curve and short-term memory were not affected in the rats although focal ischemia was induced 5 hrs before learning in either the hippocampus or the amygdala; these were impaired by the induction of ischemia in both the regions. Furthermore, the learning curve and short-term memory were impaired when ischemia was induced 24 hrs before learning in either the hippocampus or the amygdala when the synaptic transmission was altered in one region due to ischemia in the other region. These results suggest that the circuit compensation between the hippocampus and the amygdala is critical for fear memory acquisition.Significance StatementContextual fear memory needs the interconnection between the hippocampus and the amygdala. However, it is unclear whether and how the two regions produce circuit compensation under an ischemic situation. Here, we employed the developing of ischemia in the hippocampus or the amygdala or both in freely moving rats. We found that memory acquisition was not affected 5 hrs post-ischemia, but it was impaired 24 hrs post-ischemia when the synaptic transmission was impaired in one region due to ischemia in the other region. Furthermore, ischemia in both brain regions impaired memory acquisition. These results indicate a circuit compensation between the hippocampus and the amygdala in memory acquisition if one with ischemia does not affect the function of the other.