Transplantation of neural stem cells (NSCs) may be a potential strategy for traumatic brain injury treatment (TBI) due to their intrinsic advantages, such as cell replacement, secretion of neurotrophins and formation of functional synapses with host. However the underlying effects of transplanted NSCs on host micro-environment still need to be further elucidated. In this manuscript the effects of NSCs on release of neurotransmitter, survival of hippocampal neurons, reactivity of astrocytes and recovery of cognitive function after TBI were observed. The NSCs were isolated from cortex of neonatal Sprague–Dawley rat and then transplanted into injured brain regions caused by free-weight drop. The proliferation of astrocytes around injured sites were examined by GFAP immunofluorescent staining on 3, 7, 14 days after injury. The survival of neurons at CA1 regions of hippocampus toward contused regions was observed by HE staining on 3 and 14 days post-injury. The content of glutamic acid (Glu) and GABA in hippocampal tissues was examined on 1, 3, 7, 14, 28 days after injury by ELISA. On third day post-injury, hippocampal-dependent spatial memory was measured for 5 days without intermittent. NSCs in culture have the ability to proliferate and differentiate into different phenotypes of neural cells. After transplantation of NSCs, the proliferation of astrocytes around injured site was significantly inhibited compared to the injured group. At the same time the survival of neurons in hippocampal CA1 region were much more than those in injured group on 14 days post-injury. Meanwhile, the cognitive functions in NSC transplanted group was remarkably improved compared with injured group (p < 0.05). Furthermore, NSCs transplantation dramatically inhibited the release of Glu and maintained the content of GABA in injured hippocampal tissues on 1, 3, 7, 14, 28 days post-injury, which was of difference in statistics (p < 0.05). NSCs transplantation can effectively alleviate the formation of glial scar, enhance the survival of hippocampal neurons and improve cognitive function defects in rats with TBI. The underlying mechanism may be related to their effects on inhibiting the release of Glu and maintaining the content of GABA, so as to down-regulate excitotoxicity of neurotransmitter and improve the micro-environment in injured sites.

由于神经干细胞的固有优势，例如细胞置换，神经营养蛋白的分泌以及与宿主的功能性突触的形成，神经干细胞（NSCs）的移植可能是创伤性脑损伤治疗（TBI）的潜在策略。但是，仍需进一步阐明移植的NSC对宿主微环境的潜在影响。在该手稿中，观察了NSC对TBI后神经递质释放，海马神经元存活，星形胶质细胞反应性和认知功能恢复的影响。从新生Sprague–Dawley大鼠的皮层中分离出NSC，然后将其移植到由体重下降引起的受伤的大脑区域。在损伤后3、7、14天通过GFAP免疫荧光染色检查损伤部位周围星形胶质细胞的增殖。在损伤后3天和14天，通过HE染色观察海马CA1区神经元向挫伤区的存活。ELISA法在损伤后1、3、7、14、28天检查海马组织中谷氨酸（Glu）和GABA的含量。损伤后第三天，连续5天测量海马依赖性空间记忆。培养的神经干细胞能够增殖并分化为不同的神经细胞表型。与损伤组相比，NSCs移植后，损伤部位周围的星形胶质细胞增殖受到明显抑制。同时，损伤后14天，海马CA1区神经元的存活率明显高于受伤组。同时，与损伤组相比，NSC移植组的认知功能明显改善（p <0.05）。此外，NSCs移植在损伤后第1、3、7、14、28天显着抑制了受损海马组织中Glu的释放，并维持了GABA的含量，差异有统计学意义（p <0.05）。NSCs移植可以有效减轻TBI大鼠的神经胶质瘢痕的形成，提高海马神经元的存活率，改善认知功能缺陷。其潜在机制可能与其抑制Glu释放和维持GABA含量有关，从而下调神经递质的兴奋性毒性并改善受损部位的微环境。NSCs移植在损伤后第1、3、7、14、28天显着抑制了受损海马组织中Glu的释放，并维持了GABA的含量，差异有统计学意义（p <0.05）。NSCs移植可有效减轻TBI大鼠胶质瘢痕的形成，提高海马神经元的存活率，改善认知功能缺陷。其潜在机制可能与其抑制Glu释放和维持GABA含量有关，从而下调神经递质的兴奋性毒性并改善受损部位的微环境。NSCs移植在损伤后第1、3、7、14、28天显着抑制了受损海马组织中Glu的释放，并维持了GABA的含量，差异有统计学意义（p <0.05）。NSCs移植可有效减轻TBI大鼠胶质瘢痕的形成，提高海马神经元的存活率，改善认知功能缺陷。其潜在机制可能与其抑制Glu释放和维持GABA含量有关，从而下调神经递质的兴奋性毒性并改善受损部位的微环境。NSCs移植可有效减轻TBI大鼠胶质瘢痕的形成，提高海马神经元的存活率，改善认知功能缺陷。其潜在机制可能与它们抑制Glu释放并保持GABA含量有关，从而下调神经递质的兴奋性毒性并改善受损部位的微环境有关。NSCs移植可以有效减轻TBI大鼠的神经胶质瘢痕的形成，提高海马神经元的存活率，改善认知功能缺陷。其潜在机制可能与其抑制Glu释放和维持GABA含量有关，从而下调神经递质的兴奋性毒性并改善受损部位的微环境。