To further examine the inflammatory response, we stained brain sections for the microglia marker Iba-1 (Fig. 6A).
Immunohistochemistry was performed on control, JEV and JEV+M brain sections for the markers of proliferating cells: Ki-67, and PCNA.
To examine whether pericytes give rise to microglial cells in stroke, we stained brain sections for the microglial markers GAL-3, IBA1 and CD11b [ 30, 36].
To investigate if T cells are recruited to the brain following antibody-mediated neuroinflammation, we analysed brain sections for the presence of CD3 positive T cells at 24 h, 7 days and 14 days after intracerebral OVA injection.
While in each case the initial confirmatory laboratory procedure was based on the histopathologic examination of brain sections, for the most recent case (S7/CS) further investigations using IHC and WB found this animal to be affected by atypical scrapie [ 24].
To identify brain cells in which the Notch signal was activated, we stained brain sections for the Notch intracellular domain (NICD) using an antibody against the active form of Notch (Phiel et al., 2003; Ishikura et al., 2005; Palomero et al., 2006; Yang et al., 2009).
Triple label immunofluorescence staining of brain sections for galanin, GnRH and the presynaptic vesicle marker synaptophysin coupled with confocal microscopy was employed to identify galanin synapses to GnRH perikarya.
In default of an in vivo dye, we stained brain sections for hyperphosphorylated tau using the antibody AT8 (Figuire 3b-b").
To determine the appropriate brain section for assessing AEI of candidate genes, PCR amplification was first carried out using cDNA derived from purified prefrontal cortex RNA.
To assess GLP-1R expression in the brain, we immunostained brain sections for GLP-1R.
