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网络缺失加剧了视网膜变性小鼠模型的损伤。

Network deficiency exacerbates impairment in a mouse model of retinal degeneration.

机构信息

Department of Ophthalmology, Burke Medical Research Institute, Weill Medical College of Cornell University White Plains, NY, USA.

出版信息

Front Syst Neurosci. 2012 Feb 24;6:8. doi: 10.3389/fnsys.2012.00008. eCollection 2012.

Abstract

Neural oscillations play an important role in normal brain activity, but also manifest during Parkinson's disease, epilepsy, and other pathological conditions. The contribution of these aberrant oscillations to the function of the surviving brain remains unclear. In recording from retina in a mouse model of retinal degeneration (RD), we found that the incidence of oscillatory activity varied across different cell classes, evidence that some retinal networks are more affected by functional changes than others. This aberrant activity was driven by an independent inhibitory amacrine cell oscillator. By stimulating the surviving circuitry at different stages of the neurodegenerative process, we found that this dystrophic oscillator further compromises the function of the retina. These data reveal that retinal remodeling can exacerbate the visual deficit, and that aberrant synaptic activity could be targeted for RD treatment.

摘要

神经振荡在大脑的正常活动中起着重要作用,但也在帕金森病、癫痫和其他病理情况下表现出来。这些异常振荡对幸存大脑功能的贡献尚不清楚。在记录视网膜变性(RD)的小鼠模型中的视网膜时,我们发现振荡活动的发生率在不同的细胞类型之间有所不同,这表明一些视网膜网络比其他网络更容易受到功能变化的影响。这种异常活动是由一个独立的抑制性无长突细胞振荡器驱动的。通过在神经退行性过程的不同阶段刺激幸存的回路,我们发现这种营养不良的振荡器进一步损害了视网膜的功能。这些数据表明,视网膜重塑会加剧视觉缺陷,并且异常的突触活动可能成为 RD 治疗的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/3285818/848759b3edfe/fnsys-06-00008-g001.jpg

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