Supplementary Figure 8: Operant alcohol self-administration facilitated NMDAR activity and corticostriatal LTP induction in the DMS.

(a) Operant alcohol or sucrose self-administration increased the AMPAR/NMDAR ratio, as compared with age-matched water controls. Note that the data for the EtOH and sucrose groups (grey dots) are the same as in Fig. 3e and 3g, respectively. Rats in the water control group did not receive operant training. F_(2,34) = 11.13, P = 0.00019; **P < 0.01 and ***P < 0.001 versus Water; n = 13 neurons from 3 rats (Water), 13 neurons from 5 rats (EtOH), and 11 neurons from 5 rats (Sucrose). (b) Schematic illustration of the experimental procedure: After infusion of AAV-Chronos into the mPFC and AAV-Chrimson into the DMS as Fig. 3a, rats underwent operant training but without in vivo light stimulation. Twenty-four hours after the last alcohol or sucrose exposure, DMS slices were prepared. (c) Operant alcohol self-administration caused higher NMDAR activity than did operant sucrose self-administration. Comparison of input-output relation for NMDAR-EPSCs between alcohol and sucrose groups. F_{(1, 94)} = 9.62, ^##P = 0.0049; n = 13 neurons from 4 rats (Sucrose) and 13 neurons from 5 rats (EtOH). (d) Paired oHFS+oPSD induced a LTP in DMS slices from alcohol-exposed [109.66 ± 1.92% of baseline (BL), t₍₉₎ = -5.02, P = 0.00072], but not from sucrose-exposed rats [100.81 ± 1.69% of BL, t₍₆₎ = -0.48, P = 0.65; Two-sided paired t test]. ^##P = 0.0052; two-sided unpaired t test. n = 10 slices from 8 rats (EtOH) and 7 slices from 4 rats (Sucrose). One-way ANOVA followed by SNK test for a; two-way RM ANOVA followed by SNK test for c. Data are presented as mean ± s.e.m.