Fig. 6

NF-κB immunoreactivity (IR) in the choroid plexus confirms promotor-specific genetic recombination. Representative epifluorescent images of the choroid plexus (ChP) and neighboring ependyma 30 min after treatment confirms genetic recombination of Myd88 in a pattern consistent with reporter crosses (see Fig. 4a, h). In vehicle-treated (artificial cerebrospinal fluid, aCSF) control animals (Myd88 ^fl/fl, n = 3; a), clear nuclear voids of NF-κB IR are present in the cuboidal cells of the ChP (open arrowhead with asterisk) and only diffuse, cytoplasmic labeling, without concentrated nuclear labeling, is seen in the ependyma (open arrowhead). As with control animals (see Fig. 2k–l and Additional file 3: Figure S3A, B), nuclear NF-κB is evident in both cuboidal (arrowhead with asterisk in b) and ependymal cells (arrowhead in b) in response to 10 ng intracerebroventricular IL-1β treatment of TekΔMyd88 (n = 3), which do not express Cre in either cell type. In contrast, while nuclear NF-κB is present in the ependymal cells (arrowhead in c) of IL-1β-treated Slco1c1ΔMyd88 animals (n = 3), NF-κB IR remains cytoplasmic in ChP cuboidal cells where Slco1c1-Cre is expressed (arrowhead with asterisk in c; compare with Fig. 4h). Scale bars = 100 μm