首页> 外文期刊>The European Journal of Neuroscience >NR2B subunit-dependent long-term potentiation enhancement in the rat cortical auditory system in vivo following masking of patterned auditory input by white noise exposure during early postnatal life.
【24h】

NR2B subunit-dependent long-term potentiation enhancement in the rat cortical auditory system in vivo following masking of patterned auditory input by white noise exposure during early postnatal life.

机译:出生后早期白噪声暴露掩盖了模式性听觉输入后,体内大鼠皮质听觉系统中的NR2B亚单位依赖性长期增强作用增强。

获取原文
获取原文并翻译 | 示例
       

摘要

The composition of N-methyl-D-aspartate (NMDA) receptor subunits influences the degree of synaptic plasticity expressed during development and into adulthood. Here, we show that theta-burst stimulation of the medial geniculate nucleus reliably induced NMDA receptor-dependent long-term potentiation (LTP) of field postsynaptic potentials recorded in the primary auditory cortex (A1) of urethane-anesthetized rats. Furthermore, substantially greater levels of LTP were elicited in juvenile animals (30-37 days old; approximately 55% maximal potentiation) than in adult animals (approximately 30% potentiation). Masking patterned sound via continuous white noise exposure during early postnatal life (from postnatal day 5 to postnatal day 50-60) resulted in enhanced, juvenile-like levels of LTP (approximately 70% maximal potentiation) relative to age-matched controls reared in unaltered acoustic environments (approximately 30%). Rats reared in white noise and then placed in unaltered acoustic environments for 40-50 days showed levels of LTP comparable to those of adult controls, indicating that white noise rearing results in a form of developmental arrest that can be overcome by subsequent patterned sound exposure. We explored the mechanisms mediating white noise-induced plasticity enhancements by local NR2B subunit antagonist application in A1. NR2B subunit antagonists (Ro 25-6981 or ifenprodil) completely reversed white noise-induced LTP enhancement at concentrations that did not affect LTP in adult or age-matched controls. We conclude that white noise exposure during early postnatal life results in the maintenance of juvenile-like, higher levels of plasticity in A1, an effect that appears to be critically dependent on NR2B subunit activation.
机译:N-甲基-D-天冬氨酸(NMDA)受体亚基的组成会影响发育和成年后表达的突触可塑性的程度。在这里,我们显示内侧膝状核的theta-burst刺激可靠地诱导氨基甲酸酯麻醉的大鼠的主听皮层(A1)中记录的场突触后电位的NMDA受体依赖性长期增强(LTP)。此外,与成年动物(约30%的增强)相比,幼年动物(30-37天大;最大增强约55%)引起的LTP水平明显更高。在出生后早期(从出生后第5天到出生后50-60天),通过连续的白噪声暴露来掩盖模式声音,相对于未改变饲养的年龄匹配的对照组,LTP的水平增强了,类似于青少年的LTP水平(最大增强约70%)声学环境(大约30%)。以白噪声饲养的大鼠,然后在未改变的声学环境中放置40-50天,其LTP水平与成年对照组的LTP水平相当,这表明白噪声饲养导致发育停滞的形式,可以通过随后的模式声音暴露来克服。我们探索了通过局部NR2B亚基拮抗剂在A1中介导白噪声诱导的可塑性增强的机制。 NR2B亚单位拮抗剂(Ro 25-6981或ifenprodil)在不影响成年或与年龄相匹配的对照组中LTP的浓度下完全逆转了白噪声诱导的LTP增强。我们得出的结论是,在出生后早期生活中暴露于白噪声会导致维持A1的幼稚状,较高水平的可塑性,这种作用似乎主要取决于NR2B亚基的激活。

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