Alwis Dasuni Sathsara, Yan Edwin Bingbing, Johnstone Victoria, Carron Simone, Hellewell Sarah, Morganti-Kossmann Maria Cristina, Rajan Ramesh
1 Department of Physiology, Monash University , Clayton, VIC, Australia .
2 National Trauma Research Institute, Alfred Hospital , Prahran, VIC, Australia .
J Neurotrauma. 2016 Jun 1;33(11):1084-101. doi: 10.1089/neu.2014.3774. Epub 2016 Mar 23.
We have previously demonstrated that traumatic brain injury (TBI) induces significant long-term neuronal hyperexcitability in supragranular layers of sensory cortex, coupled with persistent sensory deficits. Hence, we aimed to investigate whether brain plasticity induced by environmental enrichment (EE) could attenuate abnormal neuronal and sensory function post-TBI. TBI (n = 22) and sham control (n = 21) animals were randomly assigned housing in either single or enriched conditions for 7-9 weeks. Then, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including those mimicking motion in awake animals undertaking different tasks. Long-term EE exposure (6 weeks) attenuated TBI-induced hyperexcitability in layers 2-3, such that neuronal activity in TBI animals exposed to EE was restored to control levels. Little to no EE-induced changes in population neuronal responses occurred in input layer 4 and output layer 5. However, single-cell responses demonstrated EE-induced hypoexcitation in L4 post-TBI. EE was also able to fully ameliorate sensory hypersensitivity post-TBI, although it was not found to improve motor function. Long-term enrichment post-TBI induces changes at both the population and single-cell level in the sensory cortex, where EE may act to restore the excitation/inhibition balance in supragranular cortical layers.
我们之前已经证明,创伤性脑损伤(TBI)会在感觉皮层的颗粒上层诱导显著的长期神经元过度兴奋,并伴有持续的感觉缺陷。因此,我们旨在研究环境富集(EE)诱导的脑可塑性是否能减轻TBI后的异常神经元和感觉功能。将TBI组(n = 22)和假手术对照组(n = 21)动物随机分配至单笼或富集环境中饲养7 - 9周。然后,在终末实验中,从桶状皮层神经元记录细胞外电活动以响应触须运动,包括模拟清醒动物执行不同任务时的运动。长期EE暴露(6周)减轻了TBI诱导的2 - 3层神经元过度兴奋,使得暴露于EE的TBI动物的神经元活动恢复到对照水平。在输入层4和输出层5中,几乎没有EE诱导的群体神经元反应变化。然而,单细胞反应显示TBI后EE在L4诱导了兴奋性降低。EE还能够完全改善TBI后的感觉超敏反应,尽管未发现其能改善运动功能。TBI后的长期富集在感觉皮层的群体和单细胞水平均诱导了变化,其中EE可能起到恢复颗粒上层皮质层兴奋/抑制平衡的作用。