Figure 5
Chemogenetic inactivation of the vCA1-IL pathway reversed the changes of synaptosomal GluA2, pY876 GluA2 in the IL, basal synaptic transmission, and LTD induction in vCA1-IL pathway. (a) Synaptosomal protein level of GluA2 after bilateral saline or CNO injections after context-induced reinstatement of heroin seeking. Two-way ANOVA, *P< 0.05 vs the hM4D(Gi)+CNO of ABB group; #P< 0.05 vs the hM4D(Gi)+Saline of ABB group, n=6–8 per group. (b) Ratio of pY876 GluA2/GluA2 protein levels in the IL after bilateral saline or CNO treatment after context-induced reinstatement of heroin seeking. Two-way ANOVA, *P<0.05 vs the hM4D(Gi)+CNO of ABB group; #P<0.05 vs the hM4D(Gi)+Saline of ABB group, n=6–8 per group. (c) Input–output curves, *P<0.05 vs the hM4D(Gi)+Saline of ABA group; #P<0.05 vs each stimulation intensity of hM4D(Gi)+Saline of ABA group, n=4–5 per group. (d) LTD induction in the vCA1-IL pathway after LFBS stimulation, n=4–5 per group. Representative traces at the baseline and after LFBS stimulation are shown. Calibration: vertical scale bar, 0.25 mV; horizontal scale bar, 40 ms. (e) Summary of the magnitude change of LFBS-induced LTD in each group. FP amplitude after the LFBS stimulation represented as a percent change from the baseline. Two-way ANOVA, *P<0.05 vs the hM4D(Gi)+CNO of ABB group; #P<0.05 vs the hM4D(Gi)+Saline of ABB group, n=4–5 per group. Data are depicted as the mean±SEM.
