Figure 2 | Scientific Reports

Figure 2

From: Activation of β3-adrenoceptor increases the number of readily releasable glutamatergic vesicle via activating Ca2+/calmodulin/MLCK/myosin II pathway in the prefrontal cortex of juvenile rats

Figure 2

Stimulation of β3-AR facilitates AMPAR-EPSCs via increasing pre-synaptic glutamate release. (A) Upper: A typical trace of mEPSCs recorded before (left) and during (right) the application of SR58611A (15 µM) in the presence of PTX (100 µM), AP-5 (50 µM) and TTX (1 µM) at a holding potential of − 70 mV. Lower: Time course of the SR58611A-induced increase in mEPSC frequency averaged from 7 cells. (B) Upper: Cumulative distribution of inter-event intervals and histograms showed that SR58611A (15 µM) reduced mEPSC frequency. Lower: Cumulative distribution of amplitude and histograms showed that the SR58611A (15 µM) had no effect on mEPSC amplitude. (C) SR58611A (15 µM) decreased the paired-pulse ratio (PPR = EPSC2/EPSC1, EPSC1and EPSC2 were the EPSCs evoked by two stimuli at an interval of 50 ms) of AMPAR-EPSCs. (D) SR58611A (15 µM) did not changed post-synaptic AMPA receptor-mediated currents evoked by puff application of glutamate (100 µM) in the extracellular presence of PTX (100 µM), AP-5 (50 µM), TTX (1 µM) and CTZ (10 µM). Inset indicated that bath application of AMPA receptor antagonist DNQX (25 µM) completely blocked glutamate-induced currents. *P < 0.05 vs. control. (E) Summary of experiments showed that application of SR58611A (15 µM) still significantly increased AMPAR-EPSCs amplitudes in the intracellular presence of a general G-protein inactivator GDP-β-S (1 mM).

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