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Using mice deficient in the expression of NK-1R or the prophylactic administration of the NK-1R antagonist L703,606, we have demonstrated that substance P interactions with NK-1R are required for the increases in blood-brain barrier permeability, astrogliosis, increased CNS cellularity, and elevated numbers of microglia/macrophages associated with infection with the clinically relevant bacterial CNS pathogens Streptococcus pneumoniae , Neisseria meningitidis and Borrelia burgdorferi (Chauhan et al., 2008, 2011)

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Then, plates were washed with PBS, fixed with 4% paraformaldehyde, permeabilized by 0.2% Triton X-PBS solution, repeatedly washed by PBS, and stained with FITC-labeled phalloidin to bounds with the F-actin ring in cells for 1 h in darkness

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