Novel microglia-mediated mechanisms underlying synaptic loss and cognitive impairment after traumatic brain injury

• DOI: 10.1016/j.bbi.2021.08.210
• Publication Date: 2021-08-14T14:46:24Z
• Authors: Karen Krukowski; Amber Nolan; McKenna Becker; Katherine Picard; Nathalie Vernoux; Elma S. Frias; Xi Feng; Marie-Eve Tremblay; Susanna Rosi
• Keywords: Brain damage

Traumatic brain injury (TBI) is one of the leading causes long-term neurological disability in world. Currently, there are no therapeutics for treating deleterious consequences trauma; this part due to a lack complete understanding cellular processes that underlie TBI-related pathologies. Following TBI, microglia, resident immune cells, turn into "reactive" state characterized by production inflammatory mediators contribute development cognitive deficits. Utilizing multimodal, state-of-the-art techniques widely span from ultrastructural analysis optogenetic interrogation circuit function, we investigated reactive microglia phenotype week after when learning and memory deficits also measured. Microglia displayed increased: (i) phagocytic activity vivo, (ii) synaptic engulfment, (iii) increased neuronal contact, including with dendrites somata (termed 'satellite microglia'). Functionally, satellite might impact somatic inhibition as demonstrated associated reduction inhibitory drive. Cumulatively, here demonstrate novel microglia-mediated mechanisms may loss impairment traumatic injury.