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Continuous monitoring and regulating of brain temperature in the conscious and freely moving ischemic gerbil: Effect of MK‐801 on delayed neuronal death in hippocampal CA1
Author(s) -
Zhang Long,
Mitani Akira,
Yanase Hisato,
Kataoka Kiyoshi
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19970215)47:4<440::aid-jnr9>3.0.co;2-e
Subject(s) - neuroprotection , gerbil , hypothermia , hippocampal formation , ischemia , glutamate receptor , medicine , anesthesia , brain damage , neuroscience , hippocampus , pharmacology , brain ischemia , biology , receptor
Many glutamate antagonists have been reported to have a neuroprotective effect against ischemic brain damage; however, some of them have been also reported to induce hypothermia that confers remarkable neuroprotection against the damage. In order to avoid the confounding effects of hypothermia, we assembled a telemeter‐based brain temperature control system that allows continuous monitoring and regulating of brain temperature during an ischemic insult and in the post‐ischemic period in conscious and freely moving animals. Experiments were performed in gerbils that were subjected to administration of MK‐801 (3, 5, and 10 mg/kg) and/or to 5‐min ischemia. The system monitored continuous changes in brain temperature and regulated brain temperature at normothermic levels, revealing that a neuroprotective effect of 3 mg/kg MK‐801 against ischemia‐induced delayed hippocampal CA1 neuronal death was mainly due to hypothermia, whereas a high dose of MK‐801 (5 and 10 mg/kg) produced a neuroprotective effect even when the brain temperature was maintained at normothermic levels. These results indicate that this system is very useful to test potential antiischemic agents, especially when the agents have hypothermic side effects. J. Neurosci. Res. 47:440–448, 1997. © 1997 Wiley‐Liss, Inc.