Spineless Behavior of CX3CR1+ Monocytes in Response to Infection Paul A. Muller, Daniel Mucida  Immunity  Volume 47, Issue 1, Pages 12-14 (July 2017) DOI: 10.1016/j.immuni.2017.06.022 Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 1 Poly(I:C)-Induced CX3CR1+ Monocyte-Derived TNF-α Leads to Cortical Dendritic Spine Loss and Negatively Impacts Memory Formation On the left (highlighted in blue), a wild-type mouse is trained on an accelerating rotating rod (rotarod). Following a 2-day training period, longitudinal two-photon microscopy reveals an increase in motor cortex neuronal dendritic spines as indicated by the blue arrows. At the right (highlighted in red), a wild-type mouse is injected with the viral mimetic polyinosinic-polycytidilic acid (poly(I:C)) prior to rotarod training. After the same 2-day training period, there is a decrease in the number of dendritic spines as indicated by the red arrows. In addition, the mouse shows a significant impairment in the ability to recall a recent motor memory, which is illustrated by a failure to stay on the rotarod. The decrease in spine number and memory impairment is likely the result of TNF-α secreted by CX3CRhi circulating monocytes in response to poly(I:C). Immunity 2017 47, 12-14DOI: (10.1016/j.immuni.2017.06.022) Copyright © 2017 Elsevier Inc. Terms and Conditions