Figure 1

Stimulation of β3-AR facilitates glutamatergic transmission. (A) Summary of experiments showed that SR58611A (15 µM) enhances AMPAR-EPSCs in the presence of GABAA receptor antagonist PTX (100 µM) and NMDA receptor antagonist AP-5 (50 µM) at a holding potential of − 70 mV. Sample traces were averages of ten consecutive AMPAR-EPSCs recorded at the time courses indicated by the numbers on the graph. Horizontal bars denoted the period of delivery of SR58611A. (B) Summary of experiments showed that SR58611A-induced potentiates of AMPAR-EPSCs were blocked by β3-AR antagonist SR59230A (1 µM), but not by β1-AR antagonist betaxolol (1 µM) or β2-AR antagonist ICI118551 (1 µM). (C) A SR58611A concentration–response curve. Number of neurons used was showed at the top of each group. (D) Summary of experiments showed that application of the transcriptional inhibitor, anisomycin (10 µM) failed to block SR58611A-induced increases in AMPAR-EPSCs.