Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia

To investigate the mechanism of chronic cell death following postischemic h ypothermia, the change of N-methyl-D-aspartate receptor (NMDAR! were examin ed by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in th e CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32 degrees Cx4 h), all CA1 neurons survived; however, immunore activity of NMDAR1 increased in neuronal perikarya whereas decreased in den drites in the CAL neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depres sed at 1 week after hypothermia. These results suggest that some abnormalit ies in the glutamate receptor may be caused by ischemia; such abnormality w ould persist in spite of hypothermia treatment, resulting in the depression of LTP. (C) 2000 Elsevier Science B.V. All rights reserved.