...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Brain‐derived neurotrophic factor haploinsufficiency impairs high‐frequency cortical oscillations in mice
【24h】

Brain‐derived neurotrophic factor haploinsufficiency impairs high‐frequency cortical oscillations in mice

机译：脑衍生的神经营养因子HAPloUnducks在小鼠中损害高频皮质振荡

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract Schizophrenia is a complex psychiatric disorder with a heterogeneous aetiology involving genetic and environmental factors. Deficiencies in both brain‐derived neurotrophic factor ( BDNF ) and NMDA receptor function have been implicated in the disorder and may play causal and synergistic roles. Perturbations in the regulation of electrophysiological signals, including high‐frequency (γ: 30–80?Hz and β: 20–30?Hz) neuronal oscillations, are also associated with the disorder. This study investigated the influence of BDNF deficiency and NMDA receptor hypofunction on electrophysiological responses to brief acoustic stimuli. Adult BDNF heterozygote ( BDNF +/? ) and wild‐type littermate C57Bl/6J mice were surgically implanted with EEG recording electrodes. All mice underwent EEG recording sessions to measure ongoing and auditory‐evoked electrophysiological responses following treatment with MK ‐801 (0.3?mg/kg ip) or vehicle. Western blotting on post‐mortem cortical tissue assessed parvalbumin and GAD 67 expression – markers of interneurons which are involved in the generation of gamma oscillations. Compared with wild‐type controls, BDNF +/? mice exhibited markedly dampened electrophysiological responses to auditory stimuli, including reductions in the amplitude of multiple components of the event‐related potential and auditory‐evoked oscillations, as well as reduced ongoing cortical gamma oscillations. MK ‐801 elevated ongoing gamma power but suppressed evoked gamma power, and this was observed equally across genotypes. BDNF +/? mice also displayed reductions in parvalbumin, but not GAD 67 expression. We conclude that reduced BDNF expression leads to impairments in the generation of high‐frequency neural oscillations, but this is not synergistic with NMDA receptor hypofunction. Reduced parvalbumin expression associated with BDNF haploinsufficiency may provide a molecular explanation for these electrophysiological deficits.
机译：摘要精神分裂症是一种复杂的精神疾病，具有涉及遗传和环境因素的异质性病。脑衍生的神经营养因子（BDNF）和NMDA受体功能的缺陷已经涉及该病症，并且可能发挥因果和协同作用。在电生理信号调节中的扰动，包括高频（γ：30-80≤Hz和β：20-30？Hz）神经元振荡也与这种病症有关。本研究调查了BDNF缺乏和NMDA受体的影响对短声刺激的电生理反应对电生理响应的影响。成年BDNF杂合子（BDNF + /α）和野生型凋落物C57BL / 6J小鼠用EEG记录电极手术植入。所有小鼠都接受了EEG记录会话，以测量用MK -801（0.3×mg / kg IP）或载体处理后的持续和听觉诱发的电生理学反应。 Western Blotting在验尸皮疹组织上评估的帕瓦尔蛋白酶和GAD 67表达 - 涉及伽马振荡产生的中间核标记。与野生型控制相比，BDNF + /？小鼠表现出对听觉刺激的显着抑制的电生理反应，包括减少事件相关电位和听觉诱发振荡的多个部件的幅度，以及减少的持续皮质伽马振荡。 MK -801升高的伽马功率升高，但抑制了诱发的伽马功率，这在基因型中同样观察到。 BDNF + /？小鼠还在帕瓦尔蛋白内展示减少，但不是GAD 67表达。我们得出结论，降低的BDNF表达导致高频神经振荡产生的损伤，但这并不是NMDA受体的缓冲功能的协同作用。与BDNF HaploUnficy相关的帕瓦尔白白表达减少可以为这些电生理缺陷提供分子解释。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号