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探讨轻度创伤性脑损伤后创伤后头痛小鼠模型的脑结构和功能异常。

Exploring cerebral structural and functional abnormalities in a mouse model of post-traumatic headache induced by mild traumatic brain injury.

机构信息

Department of Anesthesiology, Central People's Hospital of Zhanjiang, Zhanjiang, Guangdong 524045, China.

Key Laboratory of Nuclear Radiation and Nuclear Energy Technology, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Zool Res. 2024 May 18;45(3):648-662. doi: 10.24272/j.issn.2095-8137.2023.323.

DOI:10.24272/j.issn.2095-8137.2023.323
PMID:38766747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11188605/
Abstract

Mild traumatic brain injury (mTBI)-induced post-traumatic headache (PTH) is a pressing public health concern and leading cause of disability worldwide. Although PTH is often accompanied by neurological disorders, the exact underlying mechanism remains largely unknown. Identifying potential biomarkers may prompt the diagnosis and development of effective treatments for mTBI-induced PTH. In this study, a mouse model of mTBI-induced PTH was established to investigate its effects on cerebral structure and function during short-term recovery. Results indicated that mice with mTBI-induced PTH exhibited balance deficits during the early post-injury stage. Metabolic kinetics revealed that variations in neurotransmitters were most prominent in the cerebellum, temporal lobe/cortex, and hippocampal regions during the early stages of PTH. Additionally, variations in brain functional activities and connectivity were further detected in the early stage of PTH, particularly in the cerebellum and temporal cortex, suggesting that these regions play central roles in the mechanism underlying PTH. Moreover, our results suggested that GABA and glutamate may serve as potential diagnostic or prognostic biomarkers for PTH. Future studies should explore the specific neural circuits involved in the regulation of PTH by the cerebellum and temporal cortex, with these two regions potentially utilized as targets for non-invasive stimulation in future clinical treatment.

摘要

轻度创伤性脑损伤(mTBI)后引起的创伤后头痛(PTH)是一个紧迫的公共卫生问题,也是全球致残的主要原因。尽管 PTH 通常伴有神经紊乱,但确切的潜在机制仍知之甚少。确定潜在的生物标志物可能会促使对 mTBI 引起的 PTH 的诊断和治疗方法的开发。在这项研究中,建立了 mTBI 引起的 PTH 小鼠模型,以研究其在短期恢复过程中对大脑结构和功能的影响。结果表明,患有 mTBI 引起的 PTH 的小鼠在受伤后早期表现出平衡缺陷。代谢动力学显示,在 PTH 的早期阶段,神经递质的变化在小脑、颞叶/皮质和海马区域最为明显。此外,在 PTH 的早期阶段还进一步检测到脑功能活动和连通性的变化,特别是在小脑和颞叶皮质,表明这些区域在 PTH 的发病机制中起着核心作用。此外,我们的研究结果表明,GABA 和谷氨酸可能作为 PTH 的潜在诊断或预后生物标志物。未来的研究应该探讨小脑和颞叶皮质调节 PTH 的具体神经回路,这两个区域可能在未来的临床治疗中作为非侵入性刺激的靶点。

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