C3 缺失的小鼠海马认知表现和突触功能改变。
Altered cognitive performance and synaptic function in the hippocampus of mice lacking C3.
机构信息
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, The Sahlgrenska Academy at the University of Gothenburg, S-405 30 Gothenburg, Sweden; Institute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-405 30 Gothenburg, Sweden.
Institute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-405 30 Gothenburg, Sweden.
出版信息
Exp Neurol. 2014 Mar;253:154-64. doi: 10.1016/j.expneurol.2013.12.013. Epub 2013 Dec 28.
Previous work implicated the complement system in adult neurogenesis as well as elimination of synapses in the developing and injured CNS. In the present study, we used mice lacking the third complement component (C3) to elucidate the role the complement system plays in hippocampus-dependent learning and synaptic function. We found that the constitutive absence of C3 is associated with enhanced place and reversal learning in adult mice. Our findings of lower release probability at CA3-CA1 glutamatergic synapses in combination with unaltered overall efficacy of these synapses in C3 deficient mice implicate C3 as a negative regulator of the number of functional glutamatergic synapses in the hippocampus. The C3 deficient mice showed no signs of spontaneous epileptiform activity in the hippocampus. We conclude that C3 plays a role in the regulation of the number and function of glutamatergic synapses in the hippocampus and exerts negative effects on hippocampus-dependent cognitive performance.
先前的研究表明，补体系统在成人神经发生以及发育和损伤中枢神经系统（CNS）中的突触消除中起作用。在本研究中，我们使用缺乏第三种补体成分（C3）的小鼠来阐明补体系统在海马体依赖性学习和突触功能中的作用。我们发现，C3 的组成性缺失与成年小鼠的位置和反转学习增强有关。我们发现 CA3-CA1 谷氨酸能突触的释放概率降低，而 C3 缺乏小鼠的这些突触的整体效能不变，这表明 C3 是海马体中功能性谷氨酸能突触数量的负调节剂。C3 缺乏的小鼠在海马体中没有自发癫痫样活动的迹象。我们得出结论，C3 参与调节海马体中谷氨酸能突触的数量和功能，并对海马体依赖性认知表现产生负面影响。
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