Bibineyshvili Yelena, Vajtay Thomas J, Salsabilian Shiva, Fliss Nicholas, Suvarnakar Aastha, Fang Jennifer, Teng Shavonne, Alder Janet, Najafizadeh Laleh, Margolis David J
Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA.
Department of Electrical and Computer Engineering, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA.
Exp Physiol. 2025 Feb;110(2):321-344. doi: 10.1113/EP092219. Epub 2024 Nov 22.
Traumatic brain injury (TBI) affects neural function at the local injury site and also at distant, connected brain areas. However, the real-time neural dynamics in response to injury and subsequent effects on sensory processing and behaviour are not fully resolved, especially across a range of spatial scales. We used in vivo calcium imaging in awake, head-restrained male and female mice to measure large-scale and cellular resolution neuronal activation, respectively, in response to a mild/moderate TBI induced by focal controlled cortical impact (CCI) injury of the motor cortex (M1). Widefield imaging revealed an immediate CCI-induced activation at the injury site, followed by a massive slow wave of calcium signal activation that travelled across the majority of the dorsal cortex within approximately 30 s. Correspondingly, two-photon calcium imaging in the primary somatosensory cortex (S1) found strong activation of neuropil and neuronal populations during the CCI-induced travelling wave. A depression of calcium signals followed the wave, during which we observed the atypical activity of a sparse population of S1 neurons. Longitudinal imaging in the hours and days after CCI revealed increases in the area of whisker-evoked sensory maps at early time points, in parallel to decreases in cortical functional connectivity and behavioural measures. Neural and behavioural changes mostly recovered over hours to days in our M1-TBI model, with a more lasting decrease in the number of active S1 neurons. Our results in unanaesthetized mice describe novel spatial and temporal neural adaptations that occur at cortical sites remote to a focal brain injury.
创伤性脑损伤(TBI)会影响局部损伤部位以及远处相连脑区的神经功能。然而,损伤后实时神经动力学以及对感觉处理和行为的后续影响尚未完全明确,尤其是在一系列空间尺度上。我们对清醒、头部固定的雄性和雌性小鼠进行了体内钙成像,分别测量了运动皮层(M1)局灶性控制皮层撞击(CCI)损伤诱导的轻度/中度TBI后大规模和细胞分辨率的神经元激活情况。宽场成像显示,CCI损伤部位立即出现激活,随后在大约30秒内,钙信号激活的大量慢波穿过大部分背侧皮层。相应地,在初级体感皮层(S1)进行的双光子钙成像发现,在CCI诱导的行波期间,神经纤维网和神经元群体有强烈激活。行波之后钙信号出现抑制,在此期间我们观察到S1神经元稀疏群体的异常活动。CCI后数小时和数天的纵向成像显示,早期时间点触须诱发感觉图谱的面积增加,同时皮层功能连接性和行为指标下降。在我们的M1-TBI模型中,神经和行为变化在数小时至数天内大多恢复,但活跃的S1神经元数量有更持久的减少。我们在未麻醉小鼠中的研究结果描述了在局灶性脑损伤远处皮层部位发生的新型时空神经适应性变化。