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Titolo:
Long-term activation of the glutamatergic system associated with N-methyl-D-aspartate receptors after postischemic hypothermia in gerbils
Autore:
Nakamura, T; Miyamoto, O; Kawai, N; Negi, T; Itano, T; Nagao, S;
Indirizzi:
Kagawa Med Univ, Dept Biol, Miki, Kagawa 7610793, Japan Kagawa Med Univ Miki Kagawa Japan 7610793 ol, Miki, Kagawa 7610793, Japan Kagawa Med Univ, Dept Neurol Surg, Miki, Kagawa 7610793, Japan Kagawa Med Univ Miki Kagawa Japan 7610793 rg, Miki, Kagawa 7610793, Japan Kagawa Med Univ, Dept Basic Sports Med, Miki, Kagawa 7610793, Japan KagawaMed Univ Miki Kagawa Japan 7610793 ed, Miki, Kagawa 7610793, Japan
Titolo Testata:
NEUROSURGERY
fascicolo: 3, volume: 49, anno: 2001,
pagine: 706 - 713
SICI:
0148-396X(200109)49:3<706:LAOTGS>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT FOREBRAIN ISCHEMIA; DELAYED NEURONAL DEATH; MODERATE THERAPEUTIC HYPOTHERMIA; MICROGLIAL ACTIVATION; CIRCULATORY ARREST; CEREBRAL-ISCHEMIA; BRAIN HYPOTHERMIA; DNA FRAGMENTATION; ANEURYSM SURGERY; HIPPOCAMPUS;
Keywords:
glutamatergic activation; hypothermia; ischemia; microglia; MK-801;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Itano, T Kagawa Med Univ, Dept Biol, 1750-1 Ikenobe, Miki, Kagawa 7610793,Japan Kagawa Med Univ 1750-1 Ikenobe Miki Kagawa Japan 7610793 3, Japan
Citazione:
T. Nakamura et al., "Long-term activation of the glutamatergic system associated with N-methyl-D-aspartate receptors after postischemic hypothermia in gerbils", NEUROSURGER, 49(3), 2001, pp. 706-713

Abstract

Objective: The objective of this study was to investigate whether hypothermia would suppress secondary damage in the chronic postischemic stage, in terms of glutamate excitotoxicity. Methods: Gerbils underwent 5 minutes of ischemia via bilateral common carotid artery occlusion. Seven groups were studied, as follows: 1) ischemia without treatment group; 2) intraischemic hypothermia group; 3) postischemic hypothermia group (32 degreesC for 4 h); 4) MK-801 treatment group (2 mg/kg, every other day for 1 mo); 5) postischemic hypothermia with MK-801 treatment for I week group (2 mg/kg, every other day); 6) postischemic hypothermia with MK-801 treatment for 1 month group (2 mg/kg, every other day); and 7) sham-treated control group. One month after ischemia, histological changes in hippocampal CA1 neurons (assessed using hematoxylin and eosin staining) and memory function (assessed using an eight-arm radial maze) were studied. Extracellular glutamate concentrations were monitored by microdialysis during ischemia and hypothermia. Staining of microglia was performed 1 week and 1 month after ischemia. Results: MK-801 alone, postischemic hypothermia alone, and postischemic hypothermia with MK-801 treatment for 1 week failed to prevent ischemic neuronal damage and memory function decreases 1 month after the insult (P<0.05 versus control). However, the postischemic hypothermia with MK-801 treatmentfor 1 month group exhibited significant protective effects (not significant [P>0.05] compared with the control group). Extracellular glutamate levelsfor the intraischemic hypothermia group were significantly low, compared with the postischemic hypothermia group. There was no microglial activation in the postischemic hypothermia at 1 week and 1 month after ischemia groups. Conclusion: Postischemic hypothermia and long-term intermittent administration of MK-801 demonstrated significant neuronal protection, indicating that long-term glutamatergic activation, with changes in N-methyl-D-aspartate receptors, plays a role in neuronal damage in the chronic postischemic stage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 13:54:02