Seite - 93 - in Advances in Neuroimmunology

BrainSci. 2016,6, 25 Figure 7. Effects of the corticotropin-releasing factor 1 (CRF1R) antagonist CP154,526 (CP) on cerebro-corticalneuroimmunemRNAsfollowingrestraint stress inrats.Overall therewasasignificant effectamongthegroups forCCL2(F(2,16)=4.00,p<0.05)withCPfailing toblockstressed-induction. There alsowas aneffect of treatments forTNFα (F(2,16) = 4.87, p<0.05)with stress inducingand CPfailing toblock induction. Finally,aswithCCL2andTNFα, cortical IL-1βeffectsweresignificant overall (F(2,16)=6.34,p<0.01),but therewasnoblockadeof thestresseffectbythedrug. *p<0.05, **p<0.01versuscontrol-vehicletreatedrats.Veh=0.5%carboxymethylcellulose.A,B,and Cdelineate data forCCL2,TNFα, IL-1βandTLR4mRNAs, respectively, (n=5–7pergroup). 4.Discussion In thepresent investigation, restraint stress increased themRNAsforCCL2, IL-1β, andTNFα and the receptor TLR4 in cortex of S–D rats (Figures 2 and 3)—a result supporting a growing body of reports of acute stressor-induced increases in neuroimmune mRNAs in various brain sites [19,20,23,24,26,47]. The restraint stress-associated increase in cytokine andTLR4mRNAs in cortexpeakedbyaround4hafterexposureandthenreturnedtocontrol levelswithin1day.However, stressdidnotalwaysaffect thesemRNAsinotherbrainsites. EventhoughmRNAswere increased 93