Article Figures & Data
Figures
- Figure 1.
Alcohol causes reductions in prefrontal white matter that predict higher levels of relapse-like drinking in adulthood (Experiment 1). a, Schematic illustrating the alcohol exposure time line during adolescence and adulthood. Male rats underwent voluntary, binge self-administration sessions with sweetened alcohol (binge) or sweetened water (control) during early adolescence. In adulthood, rats were tested for baseline alcohol drinking, then exposed to chronic alcohol vapors (dependent) or ambient air (nondependent), and tested for relapse drinking (details in Gilpin et al., 2012). b, Schematic illustrating the anatomical location of CCFM and CCGenu sections. c, d, Alcohol reduced cross-sectional area of the CCFM (c; main effect of adolescent binge drinking, #p = 0.004; main effect of adult alcohol dependence, *p = 0.006), but not the CCGenu (d; all ps > 0.05). e, f, CCFM cross-sectional area did not predict baseline alcohol intake (e), but did predict the percentage increase from baseline levels after short abstinence periods, i.e., relapse-like drinking (f; p = 0.02). Data expressed as mean ± SEM (n = 4–9 rats/group).
- Figure 2.
Adolescent alcohol causes enduring damage to mPFC myelin (Experiment 1). a, Schematic illustrating the anatomical regions analyzed. b–d, Adolescent alcohol increased myelin damage, indexed by dMBP, in the gray matter just medial to the CCFM (CCFMmPFC; main effect of adolescent binge drinking, #p = 0.02). Adult dependence did not significantly increase dMBP in the CCFMmPFC (b; p > 0.05) and neither treatment significantly increased dMBP in the center of the medial branch of the CCFM (CCFMCenter; c, p > 0.05) or striatum (CCFMStriatum; d, p > 0.05). Data expressed as mean ± SEM (n = 4–9 rats/group).
- Figure 3.
Adolescent alcohol decreases myelinated fiber density in the mPFC and predicts poor T-maze performance in adulthood (Experiments 2 and 3). a, Schematic illustrating the time line of alcohol exposure during adolescence and neural and behavioral measures. Male rats underwent voluntary, binge self-administration sessions with sweetened alcohol (binge) or sweetened water (control) during early adolescence. Rats were tested on the T-maze as adolescents and again in adulthood after 6 weeks of abstinence. b, Schematic illustrating the anatomical location of the myelinated fiber density measurement (left). Alcohol reduced myelinated fiber density in the mPFC (*p = 0.002). c, There was a significant negative correlation between daily adolescent consumption and percentage correct responses in the T-maze in adulthood in binge rats (left graph; p = 0.009). This relationship was not observed in control rats (right graph; p > 0.05) and no relationships were detected between drinking behavior and T-maze performance tested in adolescence (ps > 0.05; data not shown). Data expressed as mean ± SEM (b, n = 8–9 rats/group; c, n = 13–14 rats/group).
Tables
Groups Experiment 1 Mean ± SEM Experiment 2 Mean ± SEM Experiment 3 Mean ± SEM Binge 3.21 ± 0.38 2.96 ± 0.31 Binge nondependent 4.36 ± 0.16 Binge dependent 4.52 ± 0.15 Alcohol binge consumption during adolescence (g/kg/d) for the groups in each experiment. Data shown as mean ± SEM.
