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. Author manuscript; available in PMC: 2014 Nov 1.
Published in final edited form as: Neurobiol Dis. 2013 Jul 15;59:52–62. doi: 10.1016/j.nbd.2013.07.002

FIGURE 4. THE MATURATIONAL TRAJECTORY OF RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS (RAGE) EXPRESSION IN THE YOUNG ADULT PREFRONTAL CORTEX IS DISRUPTED FOLLOWING ADOLESCENT BINGE ETHANOL EXPOSURE IN THE RAT.

FIGURE 4

(A) RAGE pixel density (×1000 Pixels/mm2) was unchanged in the adolescent prelimbic cortex (PrL) following adolescent intermittent ethanol (AIE) treatment, but was increased by 280% in the young adult, relative to CONs. (B) AIE treatment did not affect RAGE+IR in the adolescent infralimbic cortex (IL), but did increase expression by 375% in the young adult, relative to CONs. (C) AIE did not affect RAGE pixel density (×1000 Pixels/mm2) in the adolescent orbitofrontal cortex, but did increase RAGE+IR by 340% in the young adult, relative to CONs. Note: There is a maturational reduction of RAGE+IR in the CON PrL, IL, and OFC from adolescence to young adulthood. (D) Representative photomicrographs of RAGE+IR in the OFC of adolescent (P56) and young adult (P80) CON- and AIE-treated rats. Black arrowheads indicate RAGE+IR cells. Data are presented as mean ± SEM. ** indicates p<0.01, relative to CON rats. Scale bar = 50 μm.