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. 2020 Sep 23;319(6):C1097–C1106. doi: 10.1152/ajpcell.00190.2020

Fig. 2.

Fig. 2.

Corticosterone decreases solitary tract (ST)-evoked asynchronous glutamate release. A: representative recordings showing synchronous and asynchronous glutamate release during control (black traces) and following exposure to corticosterone (CORT; 1 μM; gray traces). Each trace displays five trials overlaid (shock artifact has been removed), with arrows indicating the time of ST stimulation. Inset: asynchronous excitatory post-synaptic currents (EPSCs) immediately following ST-evoked EPSCs. B: event histogram of a representative experiment showing the summed count of quantal EPSCs over time (50 trials summed, 100-ms bins). C: plot of baseline frequency of sEPSCs one second before ST-stimulation (n = 9 neurons / 5 mice). CORT decreased the number of basal spontaneous EPSCs before ST stimulation (P = 0.003, paired t test). Plots of the peak frequency (baseline subtracted) of asynchronous quantal glutamate events during a 100-ms bin (D) and area of summed asynchronous events five seconds following ST stimulation (E). CORT decreased the both peak asynchronous frequency (P < 0.001, paired t test) and the total area of the asynchronous period (P < 0.001, paired t test). F: there was no significant difference in the decay of asynchronous release (P = 0.083, using paired t test). Values are expressed as means ± SE. **P < 0.01, ***P < 0.001.