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首页> 外文期刊>BMC Neuroscience >Ketamine affects the integration of developmentally generated granule neurons in the adult stage
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Ketamine affects the integration of developmentally generated granule neurons in the adult stage

机译：氯胺酮影响成人阶段发育产生的颗粒神经元的整合

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Ketamine has been reported to cause neonatal neurotoxicity in a variety of developing animal models. Various studies have been conducted to study the mechanism of neurotoxicity for general anesthetic use during the neonatal period. Previous experiments have suggested that developmentally generated granule neurons in the hippocampus dentate gyrus (DG) supported hippocampus-dependent memory. Therefore, this study aimed to investigate whether ketamine affects the functional integration of developmentally generated granule neurons in the DG. For this purpose,the postnatal day 7 (PND-7) Sprague-Dawley (SD) rats were divided into the control group and the ketamine group (rats who received 4 injections of 40?mg/kg ketamine at 1?h intervals). To label dividing cells, BrdU was administered for three consecutive days after the ketamine exposure; NeuN+/BrdU+cells were observed by using immunofluorescence. To evaluate the developmentally generated granule neurons that support hippocampus-dependent memory, spatial reference memory was tested by using Morris Water Maze at 3?months old, after which the immunofluorescence was used to detect c-Fos expression in the NeuN+/BrdU+ cells. The expression of caspase-3 was measured by western blot to detect the apoptosis in the hippocampal DG. The present results showed that the neonatal ketamine exposure did not influence the survival rate of developmentally generated granule neurons at 2 and 3?months old, but ketamine interfered with the integration of these neurons into the hippocampal DG neural circuits and caused a deficit in hippocampal-dependent spatial reference memory tasks. In summary, these findings may promote more studies to investigate the neurotoxicity of ketamine in the developing brain.
机译：据报道，氯胺酮在各种开发动物模型中引起新生儿神经毒性。已经进行了各种研究以研究新生儿期间神经毒性神经毒性的机制。以前的实验表明，海马齿状物（DG）中的发育产生的颗粒神经元支持的海马依赖记忆。因此，该研究旨在研究氯胺酮是否影响了DG中发育产生的颗粒神经元的功能整合。为此目的，产后第7天（PND-7）Sprague-Dawley（SD）大鼠分为对照组和氯胺酮基团（在1℃间隔接受40×mg / kg氯胺酮的大鼠）。为了标记分隔细胞，在氯胺酮暴露后连续三天施用Brdu;通过使用免疫荧光观察Neun + / Brdu +细胞。为了评估支持海马依赖性存储器的发育产生的颗粒神经元，通过使用3个月大的Morris水迷宫测试空间参考记忆，之后使用免疫荧光来检测Neun + / Brdu +细胞中的C-FOS表达。通过Western印迹测量Caspase-3的表达，以检测海马DG中的凋亡。目前的结果表明，新生儿氯胺酮暴露不会影响2个月和3个月的发育生成的颗粒神经元的存活率，但氯胺酮干扰了这些神经元的整合到海马DG神经电路中并引起了海马的缺陷 - 依赖的空间参考存储器任务。总之，这些发现可以促进更多研究以研究氯胺酮在显影大脑中的神经毒性。

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