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首页> 外文期刊>IBRO Reports >Neurodegeneration in the olfactory bulb and olfactory deficits in the Ccdc66 -/- mouse model for retinal degeneration
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Neurodegeneration in the olfactory bulb and olfactory deficits in the Ccdc66 -/- mouse model for retinal degeneration

机译：视网膜变性的嗅球神经变性和Ccdc66-/-小鼠模型的嗅觉缺陷

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TheCcdc66-deficient (Ccdc66-/-) mouse model exhibits slow progressive retinal degeneration. It is unclear whether CCDC66 protein also plays a role in the wildtype (WT;Ccdc66+/+) mouse brain and whether the lack ofCcdc66gene expression in theCcdc66-/- mouse brain may result in morphological and behavioral alterations.CCDC66 protein expression in different brain regions of the adult WT mouse and in whole brain during postnatal development was quantified by SDS-PAGE and Western blot.Ccdc66reporter gene expression was visualized by X-gal staining. Selected brain regions were further analyzed by light and electron microscopy. In order to correlate anatomical with behavioral data, an olfactory habituation/dishabituation test was performed.CCDC66 protein was expressed throughout the early postnatal development in the WT mouse brain. In adult mice, the main olfactory bulb exhibited high CCDC66 protein levels comparable to the expression in the retina. Additionally, theCcdc66-/- mouse brain showed robustCcdc66reporter gene expression especially in adult olfactory bulb glomeruli, the olfactory nerve layer and the olfactory epithelium. Degeneration was detected in theCcdc66-/- olfactory bulb glomeruli at advanced age. This degeneration was also reflected in behavioral alterations; compared to the WT,Ccdc66-/- mice spent significantly less time sniffing at the initial presentation of unknown, neutral odors and barely responded to social odors.Ccdc66-/- mice develop substantial olfactory nerve fiber degeneration and alteration of olfaction-related behavior at advanced age. Thus, theCcdc66-/- mouse model for retinal degeneration adds the possibility to study mechanisms of central nervous system degeneration.
机译：Ccdc66缺陷（Ccdc66-/-）小鼠模型表现出缓慢的进行性视网膜变性。目前尚不清楚CCDC66蛋白是否也在野生型（WT; Ccdc66 + / +）小鼠脑中发挥作用，尚不清楚Ccdc66-/-小鼠脑中缺少CDc66基因表达是否会导致形态和行为改变.CCDC66蛋白在不同脑区的表达通过SDS-PAGE和Western blot定量检测成年WT小鼠和整个大脑在成年小鼠中的表达。通过X-gal染色观察Ccdc66reporter基因的表达。通过光学和电子显微镜进一步分析选定的大脑区域。为了使解剖学与行为数据相关联，我们进行了嗅觉习惯/适应测试.CCDC66蛋白在野生型小鼠大脑的整个出生后早期发育过程中都表达。在成年小鼠中，主要嗅球表现出与视网膜中的表达相当的高CCDC66蛋白水平。此外，Ccdc66-/-小鼠的大脑显示出强大的Ccdc66reporter基因表达，尤其是在成人嗅球肾小球，嗅神经层和嗅上皮中。在高龄时在Ccdc66-/-嗅球小球中检测到变性。这种退化也反映在行为改变上。与WT相比，Ccdc66-/-小鼠在最初出现未知，中性气味且几乎不响应社交气味时花费的嗅探时间显着减少。Ccdc66-/-小鼠在嗅觉神经纤维变性和嗅觉相关行为改变时会发生大量嗅觉神经变性。高龄。因此，用于视网膜变性的Ccdc66-/-小鼠模型增加了研究中枢神经系统变性机制的可能性。

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