MPTP-Induced Dopamine Depletion in Basolateral Amygdala via Decrease of D2R Activation Suppresses GABAA Receptors Expression and LTD Induction Leading to Anxiety-Like Behaviors

摘要

FIGURE 1. MPTP-induced dopamine depletion enhances presynaptic glutamate release. (A) Representative photomicrograph of TH-immunohistochemical staining in control mice (control) and MPTP-mice (MPTP). The BLA area is indicated by a white broken line (left panel). Scale bars = 1 mm. The arrows indicate TH positive fibers in BLA at high magnification. Scale bars = 50 μm. (B) Bar graphs show levels of D1R and D2R mRNA in BLA of control mice and MPTP-mice. (C) Schematic illustrating the locations of stimulating external capsule (EC) fibers and field potential recording in BLA. (D) Input–output (I/O) curve in BLA. Each point represents the group mean of the fEPSP slopes against stimulating intensities (SIs) from 0.2 to 0.7 mA. Two-way ANOVA, MPTP: F(1,84) = 15.393, p < 0.001; SI: F(5,84) = 29.953, p < 0.001; MPTP × SI: F(5,84) = 0.325, p < 0.001. ?p < 0.05 vs. control mice. (E,F) Bar graphs show the mean of fEPSP slopes (0.5 mA/SI) or PPF (75 ms IPI, %) in the slices of control mice treated with D1R antagonist SCH23390 (SCH), D2R antagonist L-sulpiride (L-su), CB1R antagonist AM251, AMPA receptor antagonist CNQX, or the co-application of L-sulpiride and CB1R agonist WIN55,212-2 (L-su/+WIN); in the slices of MPTP-mice treated with D1R agonist SKF38393 (SKF), D2R agonist quinpirole (quin), CB1R agonist WIN55,212-2 (WIN), AMPA receptor antagonist CNQX or the co-application of quinpirole and AM251 (quin/+AM251). ?p < 0.05 and ??p < 0.01 vs. control mice; ++p < 0.01 vs. control mice treated with L-su; #p < 0.05 and ##p < 0.01 vs. MPTP-mice; $p < 0.05 and $$p < 0.01 vs. MPTP-mice treated with quin.