a. Representative image of viral injection in the RMTg and recording electrode in the VTA of GAD-cre animals. b. Representative traces of evoked IPSCs in control (saline) and pain (CFA) condition represented as mean ± s.e.m.. c. PPR is persistently depressed in the condition of pain which is consistent with a higher release probability. (2way ANOVA for repeated measures; inter-pulse interval: F3, 141 = 12.32, p<0.0001; interaction (inter-pulse interval × treatment): F3,141 = 2.479, p=0.0637; Dunnett’s multiple comparisons post hoc test comparing PPR at each inter-pulse interval to the baseline: SAL, *p=0.0363; CFA, **p = 0.0022; ***p=0.0009; **** p<0.0001, n (SAL) = 24 cells from 4 rats, n (CFA) = 25 cells from 3 rats, data represented as mean ± s.e.m.) d. Schematic representation of behavioral methodology. e. Representative coronal section of RMTg Gq DREADD expressing neurons. Blue – DAPI; Red – m-Cherry (Gq DREADD); Green – GAD 67 (GABA neurons). f. Activation of GABA containing neurons in the RMTg induces decrease in the amount of 60% sucrose consumed (open bars-baseline, filled bars – 48 hours post CNO. 60% two-way ANOVA for repeated measures, time: F1, 11=4.816, p=0.0506; interaction (time × treatment): F1, 11=2.786, p=0.1233; Sidak’s post hoc within group: hM3Dq (n=7) baseline versus 48 hours post CNO, * p=0.0317). g. Activation of GABA containing neurons in the RMTg induces decrease in the amount of 5% sucrose consumed (open bars-baseline, filled bars – 48 hours post CNO. 5% two-way ANOVA for repeated measures, time: F1, 11=0.3548, p=0.5635; interaction (time × treatment): F1, 11=10.96, p=0.0069; Sidak’s post hoc within group: hM3Dq (n=7) baseline versus 48 hours post CNO, * p=0.03). h. Schematic representation of behavioral methodology. i. Representative coronal section of RMTg Gi DREADD expressing neurons. Blue – DAPI; Red – m-Cherry (Gi DREADD); Green – GAD 67 (GABA neurons). j. Inhibition of RMTg-VTA GABAergic pathway restores sucrose consumption in CFA treated animals. (open bars-baseline, filled bars – 48 hours (CNO) and 72 hours (VEH) post CFA). two-way ANOVA for repeated measures, time: F2, 40=28.60, p<0.0001; interaction (time × treatment): F4,40=6.707, p=0.0003; Sidak’s post hoc within group: hM3Di + CFA baseline(n=8) versus hM3Di + CFA + VEH (n=8), **** p<0.0001; hM3Di + CFA + CNO(n=8) versus hM3Di + CFA + VEH (n=8), *** p=0.0002; m-Cherry + CFA baseline(n=8) versus m-Cherry + CFA + CNO(n=8) ), **** p<0.0001; m-Cherry + CFA baseline(n=8) versus m-Cherry + CFA + VEH(n=8) ), **** p<0.0001). k. Inhibition of RMTg-VTA GABAergic pathway does not alter CFA induced hyperalgesia. (two-way ANOVA for repeated measures, time: F2, 40 = 53.58, p<0.0001; interaction (time × treatment): F4, 40 = 13.19, p<0.0001; Sidak’s post hoc for each group as compared to the group’s baseline session: **** p<0.0001). The data are presented as the mean ± s.e.m.