Figure 3

SR58611A-enhanced glutamate release requires the involvement of the Ca²⁺ /calmodulin/MLCK/myosin II pathway. (A) Bath application of BAPTA-AM (100 µM), a selective chelator of Ca²⁺, blocked SR58611A-induced augmentation of mEPSC frequency. (B) Intracellular perfusion of BAPTA-AM (100 µM) via the recording pipettes did not influence SR58611A-mediated augmentation of mEPSC frequency. (C) Bath application of the sarcoplasmic reticulum Ca²⁺-ATPase inhibitor thapsigargin (10 µM) did not abolish SR58611A-induced enhancement of mEPSC frequency. (D) Bath application of the L-type Ca²⁺ channel inhibitor nimodipine (10 µM) abolished SR58611A-enhanced mEPSC frequency. (E) Bath application of another L-type Ca²⁺ channel blocker verapamil (10 µM) counteracted SR58611A-induced increases in mEPSC frequency. (F) Bath application of the calmodulin inhibitor W7 (50 µM) blocked SR58611A-induced increases in mEPSC frequency. (G) Bath application of the MLCK inhibitor wortmannin (10 µM) blocked SR58611A-induced increases in mEPSC frequency. (H) Bath application of the ML-9 (10 µM), another MLCK inhibitor, abolished SR58611A-induced increases in mEPSC frequency. (I) Bath application of a general myosin inhibitor BHC (1 µM) blocked SR58611A-induced increases in mEPSC frequency. (J) Bath application of a specific myosin II inhibitor blebbistatin (1 µM) abolished SR58611A-induced increases in mEPSC frequency.