Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia.
To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32 degrees Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP.
Miyamoto
O
O
Department of Biology, Kagawa Medical University, Miki-cho, Japan.
Nakamura
T
T
Yamagami
S
S
Negi
T
T
Tokuda
M
M
Matsui
H
H
Itano
T
T
D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D002470:Cell Survival; D005849:Gerbillinae; D006624:Hippocampus / Q000503:physiopathology*; D006979:Hyperthermia, Induced; D007150:Immunohistochemistry; D017774:Long-Term Potentiation; D008297:Male; D009474:Neurons / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D015424:Reperfusion
D016194:Receptors, N-Methyl-D-Aspartate