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首页> 外文期刊>Epilepsia: Journal of the International League against Epilepsy >Halothane as a neuroprotectant during constant stimulation of the perforant path.
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Halothane as a neuroprotectant during constant stimulation of the perforant path.

机译:氟烷在持续刺激穿孔路径期间作为神经保护剂。

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PURPOSE: To determine the neuroprotective effects of halothane during constant stimulation of the perforant path. METHODS: Male Sprague-Dawley rats had electrodes implanted into the perforant path and dentate granule cell layer under halothane anaesthesia (1-2% in oxygen). They were then divided into four groups. In group 1 (n = 9), the perforant path was stimulated at 20 Hz for 2 h under halothane anaesthesia (1-2%). In group 2 (n = 3), the animals were unstimulated but maintained under halothane anaesthesia (1-2%) for 2 h with the electrodes in place. Both groups 1 and 2 had the electrodes removed and were then allowed to recover fully from the anaesthetic. In groups 3 and 4, the electrodes were held in place with dental acrylic. Both of these groups were allowed to recover fully from anaesthesia. In group 3 (n = 3), 24-48 h after recovery from anaesthesia, the perforant path was stimulated at 20 Hz for 2 h. Group 4 (n = 3) received no stimulation. After 14-17 days, the rats were killed, and morphometry and cell counts were performed on the hippocampi from rats in groups 1 and 2. RESULTS: Cell densities were not significantly different between control (group 2), unstimulated rats, and animals stimulated under halothane anaesthesia (group 1). Stimulation in the unanaesthetised rats resulted in severe neuronal loss in hilus, CA1, and CA3. CONCLUSIONS: Halothane protects hippocampal neurons against damage induced by constant stimulation of the perforant path.
机译:目的:确定在持续刺激穿孔路径过程中氟烷的神经保护作用。方法:雄性Sprague-Dawley大鼠在氟烷麻醉下(氧含量为1-2%)将电极植入穿孔路径,并形成齿状颗粒细胞层。然后将他们分为四组。在第1组(n = 9)中,在氟烷麻醉下(1-2%)以20 Hz刺激2 h。第2组(n = 3)中,未刺激动物,但在氟烷麻醉下(1-2%)将电极放置在适当位置2小时。第1组和第2组均去除了电极,然后从麻醉剂中完全恢复。在第3和第4组中,电极用牙科丙烯酸树脂固定在适当的位置。这两个组均被允许从麻醉中完全恢复。在第3组(n = 3)中,从麻醉中恢复24-48小时后,穿孔路径以20 Hz刺激了2小时。第4组(n = 3)没有受到刺激。 14-17天后,处死大鼠,对第1组和第2组大鼠的海马进行形态学和细胞计数。结果:对照组(第2组),未刺激的大鼠和受刺激的动物之间的细胞密度没有显着差异。氟烷麻醉下(第1组)。未麻醉大鼠的刺激导致hilus,CA1和CA3严重神经元丢失。结论:氟烷保护海马神经元免受持续刺激穿孔路径引起的损伤。

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