Bisht Kanchan, Sharma Kaushik, Lacoste Baptiste, Tremblay Marie-Ève
Axe Neurosciences, CRCHU de Québec , Québec City, QC, Canada.
Department of Cellular & Molecular Medicine, Faculty of Medicine, The University of Ottawa Brain and Mind Research Institute, Ottawa, ON, Canada; Neuroscience Program, The Ottawa Hospital Research Institute, Ottawa, ON, Canada.
Commun Integr Biol. 2016 Oct 3;9(6):e1230575. doi: 10.1080/19420889.2016.1230575. eCollection 2016.
Using transmission electron microscopy (TEM) we recently characterized a microglial phenotype that is induced by chronic stress, fractalkine receptor deficiency, aging, or Alzheimer disease pathology. These 'dark' microglia appear overly active compared with the normal microglia, reaching for synaptic clefts, and extensively engulfing pre-synaptic axon terminals and post-synaptic dendritic spines. From these findings we hypothesized that dark microglia could be specifically implicated in the pathological remodeling of neuronal circuits, which impairs learning, memory, and other essential cognitive functions. In the present addendum we further discuss about the possible causes of their dark appearance under TEM.
最近,我们利用透射电子显微镜(TEM)对一种由慢性应激、趋化因子受体缺乏、衰老或阿尔茨海默病病理所诱导的小胶质细胞表型进行了表征。与正常小胶质细胞相比,这些“暗”小胶质细胞显得过度活跃,它们伸向突触间隙,并广泛吞噬突触前轴突终末和突触后树突棘。基于这些发现,我们推测暗小胶质细胞可能特别参与了神经回路的病理性重塑,而这会损害学习、记忆和其他重要的认知功能。在本附录中,我们将进一步讨论它们在透射电子显微镜下呈现暗外观的可能原因。