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首页> 外文期刊>Brain structure & function >Sequential [F-18]FDG A mu PET whole-brain imaging of central vestibular compensation: a model of deafferentation-induced brain plasticity
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Sequential [F-18]FDG A mu PET whole-brain imaging of central vestibular compensation: a model of deafferentation-induced brain plasticity

机译:[F-18] FDG A mu PET全脑中央前庭补偿的影像学:去力诱发脑可塑性的模型

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摘要

Unilateral inner ear damage is followed by a rapid behavioural recovery due to central vestibular compensation. In this study, we utilized serial [F-18]Fluoro-deoxyglucose ([F-18]FDG)-A mu PET imaging in the rat to visualize changes in brain glucose metabolism during behavioural recovery after surgical and chemical unilateral labyrinthectomy, to determine the extent and time-course of the involvement of different brain regions in vestibular compensation and test previously described hypotheses of underlying mechanisms. Systematic patterns of relative changes of glucose metabolism (rCGM) were observed during vestibular compensation. A significant asymmetry of rCGM appeared in the vestibular nuclei, vestibulocerebellum, thalamus, multisensory vestibular cortex, hippocampus and amygdala in the acute phase of vestibular imbalance (4 h). This was followed by early vestibular compensation over 1-2 days where rCGM re-balanced between the vestibular nuclei, thalami and temporoparietal cortices and bilateral rCGM increase appeared in the hippocampus and amygdala. Subsequently over 2-7 days, rCGM increased in the ipsilesional spinal trigeminal nucleus and later (7-9 days) rCGM increased in the vestibulocerebellum bilaterally and the hypothalamus and persisted in the hippocampus. These systematic dynamic rCGM patterns during vestibular compensation, were confirmed in a second rat model of chemical unilateral labyrinthectomy by serial [F-18]FDG-A mu PET. These findings show that deafferentation-induced plasticity after unilateral labyrinthectomy involves early mechanisms of re-balancing predominantly in the brainstem vestibular nuclei but also in thalamo-cortical and limbic areas, and indicate the contribution of spinocerebellar sensory inputs and vestibulocerebellar adaptation at the later stages of behavioural recovery.
机译:单侧内耳损伤后由于中央前庭补偿而使行为迅速恢复。在这项研究中,我们利用大鼠中的系列[F-18]氟脱氧葡萄糖([F-18] FDG)-A mu PET成像来观察手术和化学性单侧迷路切除术后行为恢复期间脑葡萄糖代谢的变化,以确定不同的大脑区域参与前庭补偿的程度和时程,并测试先前描述的潜在机制假设。前庭代偿期间观察到葡萄糖代谢(rCGM)相对变化的系统模式。在前庭失衡的急性期,前庭核,前庭小脑,丘脑,多感觉前庭皮质,海马和杏仁核中出现rCGM的显着不对称性。随后是1-2天的早期前庭补偿,其中rCGM在前庭核,丘脑和颞顶皮质之间重新平衡,并且双侧rCGM出现在海马和杏仁核中。随后在2-7天之内,同侧脊柱三叉神经核的rCGM升高,随后(7-9天),双侧前庭小脑和下丘脑的rCGM升高,并持续存在于海马体中。在通过序列[F-18] FDG-A mu PET在化学单侧迷路切除术的第二只大鼠模型中证实了前庭补偿期间的这些系统性动态rCGM模式。这些发现表明,单侧迷路切除术后去力失力诱导的可塑性涉及主要在脑干前庭核以及丘脑皮质和边缘区重新平衡的早期机制,并表明脊髓小脑感觉输入和前庭小脑适应的贡献。行为恢复。

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