Network deficiency exacerbates impairment in a mouse model of retinal degeneration.
Network deficiency exacerbates impairment in a mouse model of retinal degeneration.
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DOI：
10.3389/fnsys.2012.00008
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发表时间：
2012
影响因子：
3
通讯作者：
Sagdullaev BT
中科院分区：
文献类型：
--
作者：
Yee CW;Toychiev AH;Sagdullaev BT
神经振荡在正常的大脑活动中起着重要作用，但也在帕金森病，癫痫和其他病理条件下表现出来。这些异常振荡对幸存大脑功能的贡献仍不清楚。在视网膜变性（RD）小鼠模型的视网膜记录中，我们发现振荡活动的发生率在不同的细胞类别中各不相同，这表明某些视网膜网络比其他网络更受功能变化的影响。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。通过刺激神经退行性过程不同阶段的幸存电路，我们发现这种营养不良振荡器进一步损害了视网膜的功能。这些数据表明，视网膜重塑可以加剧视觉缺陷，并且异常的突触活动可以被靶向用于RD治疗。
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.