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. 2013 Sep 3;7:157. doi: 10.3389/fnins.2013.00157

Figure 2.

Figure 2

Microglial activation via scratch wounding and LPS. (A) Microglial CD11b in 3 zones (1 mm wide) progressively decreased distal to the wound. Pgrmc1 protein was also induced by scratch wounding. *** p < 0.0001; ** p < 0.03; * p < 0.05 vs non-wounded. (B) CD11b and Pgrmc1 protein were both induced by by LPS. *** p < 0.0001; ** p < 0.001 vs vehicle. (C) Model to show targets of the undefined soluble activity (SA) from activated microglia and microglial Pgrmc1 that mediate the antagonism of P4 on E2-dependent neurite outgrowth. Microglial activation by LPS is assumed to be mediated by toll-like receptor-4 (TLR4); activation by scratch wounding has undefined pathways. The schema shows two possible SA actions on neurites: direct effects (solid red lines) on neurite outgrowth at the neurite growth cone (arrowhead) and/or involving the neuronal nucleus; indirect effects (dashed green lines) via astrocyte secretions on neurite or neuronal nucleus. Glial activation by injury or LPS and the SA effects were blocked by Pgrmc1 knockdown. Modified from Bali et al. (2013).