Diffuse traumatic brain injury initially attenuates and later expands activation of the rat somatosensory whisker circuit concomitant with neuroplastic responses.
Diffuse traumatic brain injury initially attenuates and later expands activation of the rat somatosensory whisker circuit concomitant with neuroplastic responses.
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DOI：
10.1016/j.brainres.2010.01.067
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发表时间：
2010-04-06
期刊：
影响因子：
2.9
通讯作者：
Lifshitz, Jonathan
中科院分区：
文献类型：
--
作者：
Hall, Kelley D.;Lifshitz, Jonathan
创伤性脑损伤可引发一系列慢性神经功能缺损，影响执行功能、语言和感觉运动整合。机械力会产生扩散性病变，破坏脆弱大脑区域的神经回路激活。本手稿探讨的假设，即脑损伤电路的功能激活的程度是最初的中断和随后的重组的结果。在大鼠中，对胡须刺激的持久感觉敏感性将区域分析引导到胡须-桶电路。成年雄性大鼠进行中线液压冲击脑或假损伤，并在损伤后1天和42天之间进行评估。通过尼氏染色可见，皮质和丘脑的须状体感区保持细胞组成。在损伤后的第一周内，晶须刺激引起的cFos激活数量较少，这可能是由于通过淀粉样前体蛋白免疫组织化学观察到的晶须回路内和周围的轴突切断。损伤后6周，胡须刺激后的cFos激活在皮质中显示出与时间的显著线性相关性（r2=0.545; p = 0.015），在丘脑中无显著相关性（r2=0.326），在齿状回中呈U形相关性（r2=0.831），所有这些最终都超过了假手术水平。皮质中正在进行的神经可塑性反应通过积累生长相关蛋白和突触素基因表达来证明。在丘脑中，可塑性标志物的延迟恢复可以解释在触须刺激下延伸到纹状体和海马的神经元激活的广泛分布。扩散性损伤的回路发芽到扩散性损伤的组织中可能建立了导致行为病态的适应不良回路。治疗干预，以促进适应性电路重建可能会减轻创伤后发病率。
Traumatic brain injury can initiate an array of chronic neurological deficits, effecting executive function, language and sensorimotor integration. Mechanical forces produce the diffuse pathology that disrupts neural circuit activation across vulnerable brain regions. The present manuscript explores the hypothesis that the extent of functional activation of brain-injured circuits is a consequence of initial disruption and consequent reorganization. In the rat, enduring sensory sensitivity to whisker stimulation directs regional analysis to the whisker-barrel circuit. Adult, male rats were subjected to midline fluid percussion brain or sham injury and evaluated between 1d and 42d post-injury. Whisker somatosensory regions of the cortex and thalamus maintained cellular composition as visualized by Nissl stain. Within the first week post-injury, quantitatively less cFos activation was elicited by whisker stimulation, potentially due to axotomy within and surrounding the whisker circuit as visualized by amyloid precursor protein immunohistochemistry. Over six weeks post-injury, cFos activation after whisker stimulation showed a significant linear correlation with time in the cortex (r2=0.545; p = 0.015), non-significant correlation in the thalamus (r2=0.326) and U-shaped correlation in the denate gyrus (r2=0.831), all eventually exceeding sham levels. Ongoing neuroplastic responses in the cortex are evidenced by accumulating growth associated protein and synaptophysin gene expression. In the thalamus, the delayed restoration of plasticity markers may explain the broad distribution of neuronal activation extending into the striatum and hippocampus with whisker stimulation. The sprouting of diffuse-injured circuits into diffuse-injured tissue likely establishes maladaptive circuits responsible for behavioral morbidity. Therapeutic interventions to promote adaptive circuit restructuring may mitigate post-traumatic morbidity.
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DOI：
10.1083/jcb.142.5.1313
发表时间：
1998-09-07
期刊：
The Journal of cell biology
影响因子：
--
作者：
Franklin JL;Johnson EM
通讯作者：
Johnson EM
影响因子：
5.3
作者：
Jain, Neeraj;Qi, Hui-Xin;Collins, Christine E.;Kaas, Jon H.
通讯作者：
Kaas, Jon H.
影响因子：
15.9
作者：
DeBello, William M.
通讯作者：
DeBello, William M.
影响因子：
12.7
作者：
Christman, CW;Salvant, JB;Povlishock, JT
通讯作者：
Povlishock, JT
影响因子：
16.2
作者：
DOSTER, SK;LOZANO, AM;WILLARD, MB
通讯作者：
WILLARD, MB