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失 prestin 并不改变听觉皮质树突棘的发育。

Loss of prestin does not alter the development of auditory cortical dendritic spines.

机构信息

Program in Neuroscience, Harvard University, Cambridge, MA 02138, USA.

出版信息

Neural Plast. 2011;2011:305621. doi: 10.1155/2011/305621. Epub 2011 May 15.

Abstract

Disturbance of sensory input during development can have disastrous effects on the development of sensory cortical areas. To examine how moderate perturbations of hearing can impact the development of primary auditory cortex, we examined markers of excitatory synapses in mice who lacked prestin, a protein responsible for somatic electromotility of cochlear outer hair cells. While auditory brain stem responses of these mice show an approximately 40 dB increase in threshold, we found that loss of prestin produced no changes in spine density or morphological characteristics on apical dendrites of cortical layer 5 pyramidal neurons. PSD-95 immunostaining also showed no changes in overall excitatory synapse density. Surprisingly, behavioral assessments of auditory function using the acoustic startle response showed only modest changes in prestin KO animals. These results suggest that moderate developmental hearing deficits produce minor changes in the excitatory connectivity of layer 5 neurons of primary auditory cortex and surprisingly mild auditory behavioral deficits in the startle response.

摘要

发育过程中感觉输入的干扰可能对感觉皮质区的发育产生灾难性的影响。为了研究中度听力干扰如何影响初级听觉皮层的发育,我们研究了缺乏 prestin 的小鼠(一种负责耳蜗外毛细胞体电动的蛋白质)中的兴奋性突触标记物。虽然这些小鼠的听觉脑干反应显示阈值增加了约 40 分贝,但我们发现 prestin 的缺失并没有改变皮质第 5 层锥体神经元顶树突上的棘密度或形态特征。PSD-95 免疫染色也显示整体兴奋性突触密度没有变化。令人惊讶的是,使用声惊反射的听觉功能行为评估显示 prestin KO 动物仅有轻微变化。这些结果表明,中度发育性听力缺陷仅在初级听觉皮层第 5 层神经元的兴奋性连接中产生较小的变化,并且在声惊反射中的听觉行为缺陷也非常轻微。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29df/3134106/8054fae06dd5/NP2011-305621.001.jpg

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