Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia. 1091 27

Hypothermia may afford histological neuroprotection induced by ischemia by preventing aberrant Ca2+ influx through NMDA (N-methyl-D-aspartic acid) or Ca2+-permeable AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) receptors. Expression of hippocampal GluR1A, GluR2B, GluR3C and NMDAR1 (NR1) subunits was investigated by in situ hybridization at 1 and 7 days after 10-min transient global ischemia in the presence and absence of intraischemic or postischemic brain hypothermia (30 degrees C). At 1 day, normothermic ischemia markedly suppressed the expression of GluR1A, GluR2B, and GluR3C receptor mRNAs to a similar degree in the vulnerable CA1. Less vulnerable CA3a-c subregions were also acutely downregulated. NR1 mRNA expression was reduced in CA1 but to a lesser extent than AMPA mRNAs. At 7 days after normothermic ischemia, a time of marked CA1 cell loss, all three AMPA transcripts were nearly absent in CA1 while a percentage (33.9+/-7.2%) of NR1 mRNA remained. Intraischemic hypothermia fully blocked the damage and non-selective mRNA downregulations at 1 and 7 days. By contrast, postischemic hypothermia postponed neurodegeneration but only partially rescued the expression of AMPA and NR1 mRNAs at 7 days and not at 1 day after the insult. Therefore, hippocampal AMPA receptor mRNAs decline at a relatively similar rate after normothermic global ischemia and cellular neuroprotection by intraischemic hypothermia occurred independently of altered subunit composition of AMPA receptors. Since decreases persist within resistant neurons under the postischemic condition, AMPA receptor-mediated Ca2+ currents probably do not contribute to selective vulnerability.
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PMID:Intraischemic but not postischemic hypothermia prevents non-selective hippocampal downregulation of AMPA and NMDA receptor gene expression after global ischemia. 1116 69

We investigated the neuroprotective efficacy of hypothermia after status epilepticus (SE) in immature rats. In addition, the expression levels of NMDAR1 and c-Jun were measured to establish a possible signaling mechanism for hypothermia-induced neuroprotection. Pilocarpine-treated rats were randomly divided into 2 groups: group D (diazepam) and group DH (diazepam plus hypothermia). Compared to the control (group NS) rats, Pilocarpine-induced SE significantly enhanced the expression of NMDAR1 and c-Jun in the hippocampus, and also significantly increased the numbers of necrotic and apoptotic pyramidal neurons. The DH group exhibited significantly fewer necrotic and apoptotic hippocampal pyramidal neurons and reduced NMDAR1 expression than group D. In contrast, early expression of c-Jun was significantly higher in the hippocampi of hypothermia-treated rats than in the hippocampi of group D, while late c-Jun expression was significantly lesser than group D. Our results show mild post-ictal hypothermia partially rescues neuronal cell death in the hippocampus following SE. We further suggest that elevated NMDAR1 expression exacerbates SE-induced neuronal death in pilocarpine-treated rats, while early c-Jun overexpression, concomitant with hypothermia, suppresses subsequent neuronal death.
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PMID:Effects of hypothermia on brain injury induced by status epilepticus. 2220 42