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纹状体损伤会在大脑皮质、丘脑和小脑水平引发全脑改变。

Striatal Injury Induces Overall Brain Alteration at the Pallial, Thalamic, and Cerebellar Levels.

作者信息

Lukacova Kristina, Hamaide Julie, Baciak Ladislav, Van der Linden Annemie, Kubikova Lubica

机构信息

Institute of Animal Biochemistry and Genetics, Centre of Biosciences, Slovak Academy of Sciences, 840 05 Bratislava, Slovakia.

Bio-Imaging Laboratory, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, B-2610 Antwerp, Belgium.

出版信息

Biology (Basel). 2022 Mar 10;11(3):425. doi: 10.3390/biology11030425.

Abstract

The striatal region Area X plays an important role during song learning, sequencing, and variability in songbirds. A previous study revealed that neurotoxic damage within Area X results in micro and macrostructural changes across the entire brain, including the downstream dorsal thalamus and both the upstream pallial nucleus HVC (proper name) and the deep cerebellar nuclei (DCN). Here, we specify these changes on cellular and gene expression levels. We found decreased cell density in the thalamic and cerebellar areas and HVC, but it was not related to neuronal loss. On the contrary, perineuronal nets (PNNs) in HVC increased for up to 2 months post-lesion, suggesting their protecting role. The synaptic plasticity marker Forkhead box protein P2 (FoxP2) showed a bi-phasic increase at 8 days and 3 months post-lesion, indicating a massive synaptic rebuilding. The later increase in HVC was associated with the increased number of new neurons. These data suggest that the damage in the striatal vocal nucleus induces cellular and gene expression alterations in both the efferent and afferent destinations. These changes may be long-lasting and involve plasticity and neural protection mechanisms in the areas directly connected to the injury site and also to distant areas, such as the cerebellum.

摘要

纹状体区域X在鸣禽的歌曲学习、序列生成和变异性过程中发挥着重要作用。先前的一项研究表明,X区域内的神经毒性损伤会导致整个大脑的微观和宏观结构变化,包括下游的背侧丘脑以及上游的 pallial 核HVC(专有名称)和小脑深部核团(DCN)。在此,我们在细胞和基因表达水平上明确了这些变化。我们发现丘脑、小脑区域和HVC中的细胞密度降低,但这与神经元损失无关。相反,损伤后长达2个月,HVC中的神经元周围网络(PNNs)增加,表明它们具有保护作用。突触可塑性标记物叉头框蛋白P2(FoxP2)在损伤后8天和3个月呈现双相增加,表明存在大规模的突触重建。HVC中后期的增加与新神经元数量的增加有关。这些数据表明,纹状体发声核团的损伤会在传出和传入目标区域诱导细胞和基因表达改变。这些变化可能是持久的,并且涉及与损伤部位直接相连的区域以及诸如小脑等远处区域的可塑性和神经保护机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1383/8945699/82cf231b9cfd/biology-11-00425-g001.jpg

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