Ouyang Wei, Yan Qichao, Zhang Yu, Fan Zhiheng
College of Physical Education and Health Sciences, Zhejiang Normal University, Jinhua, Zhejiang, China.
Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi, China.
PLoS One. 2017 Feb 14;12(2):e0171976. doi: 10.1371/journal.pone.0171976. eCollection 2017.
Moderate traumatic brain injury (TBI) in children often happen when there's a sudden blow to the frontal bone, end with long unconscious which can last for hours and progressive cognitive deficits. However, with regard to the influences of moderate TBI during children adulthood, injury-induced alterations of locomotive ability, long-term memory performance, and hippocampal electrophysiological firing changes have not yet been fully identified. In this study, lateral fluid percussion (LFP) method was used to fabricate moderate TBI in motor and somatosensory cortex of the 6-weeks-old mice. The motor function, learning and memory function, extracellular CA1 neural spikes were assessed during acute and subacute phase. Moreover, histopathology was performed on day post injury (DPI) 16 to evaluate the effect of TBI on tissue and cell morphological changes in cortical and hippocampal CA1 subregions. After moderate LFP injury, the 6-weeks-old mice showed severe motor deficits at the early stage in acute phase but gradually recovered later during adulthood. At the time points in acute and subacute phase after TBI, novel object recognition (NOR) ability and spatial memory functions were consistently impaired in TBI mice; hippocampal firing frequency and burst probability were hampered. Analysis of the altered burst firing shows a clear hippocampal theta rhythm drop. These electrophysiological impacts were associated with substantially lowered NOR preference as compared to the sham group during adulthood. These results suggest that moderate TBI introduced at motorsenory cortex in 6-weeks-old mice causes obvious motor and cognitive deficits during their adulthood. While the locomotive ability progressively recovers, the cognitive deficits persisted while the mice mature as adult mice. The cognitive deficits may be attributed to the general suppressing of whole neural network, which could be labeled by marked reduction of excitability in hippocampal CA1 subregion.
儿童中度创伤性脑损伤（TBI）通常发生在额骨受到突然撞击时，以长时间昏迷（可持续数小时）和进行性认知缺陷告终。然而，关于中度TBI对儿童成年期的影响，损伤引起的运动能力改变、长期记忆表现以及海马体电生理放电变化尚未完全明确。在本研究中，采用侧脑室液体冲击（LFP）方法在6周龄小鼠的运动和体感皮层制造中度TBI。在急性期和亚急性期评估运动功能、学习和记忆功能以及细胞外CA1神经尖峰。此外，在损伤后第16天进行组织病理学检查，以评估TBI对皮层和海马体CA1亚区组织和细胞形态变化的影响。中度LFP损伤后，6周龄小鼠在急性期早期表现出严重的运动缺陷，但在成年后期逐渐恢复。在TBI后的急性期和亚急性期时间点，TBI小鼠的新物体识别（NOR）能力和空间记忆功能持续受损；海马体放电频率和爆发概率受到阻碍。对改变的爆发性放电分析显示海马体θ节律明显下降。与成年期假手术组相比，这些电生理影响与NOR偏好显著降低有关。这些结果表明，6周龄小鼠运动感觉皮层的中度TBI在其成年期会导致明显的运动和认知缺陷。虽然运动能力逐渐恢复，但随着小鼠成年，认知缺陷仍然存在。认知缺陷可能归因于整个神经网络的普遍抑制，这可以通过海马体CA1亚区兴奋性的显著降低来标记。
