Chronic stress reduces exNMDAR functions. (A)
Left: Histograms of normalized weight gain of control (n = 7) and chronically stressed rats (n = 8) in 21 days. Right: Histograms of CORT levels in trunk blood in control (n = 7) and chronically stressed rats (n = 8) collected right before brain slice preparation. Stressed rats were sacrificed 7 days within the end of chronic restraint stress. Mean ± SEM. *p < 0.05, **p < 0.01, Student’s t-test. (B)
Left: Representative traces of evoked NMDAR-mediated field excitatory postsynaptic potential (fEPSP) that were recorded from brain slices of control and chronically stressed rats. Scale bar = 0.2 mV, 40 ms. Right: Scatter plots show the relationship between fiber volley amplitude and the slope of NMDAR fEPSP in control (7 recordings, 4 rats) and stressed rats (8 recordings, 4 rats). Mean ± SEM. (C)
Left: Representative traces of evoked AMPAR-mediated fEPSP that were recorded from brain slices of control and chronically stressed rats. Scale bar = 0.4 mV, 25 ms. Right: Scatter plots show the relationship between fiber volley amplitude and the slope of AMPAR fEPSP in control (10 recordings, 4 rats) and stressed rats (13 recordings, 4 rats). Mean ± SEM. (D)
Left: Representative traces of sNMDAR and TBOA-induced exNMDAR currents from brain slices of control or chronically stressed rats. Scale bar = 50 pA, 500 ms. Right: Histogram shows the normalized amplitude of exNMDAR currents recorded from brain slices of control (5 recordings, 4 rats) and chronically stressed rats (7 recordings, 6 rats). Mean ± SEM. *p < 0.05, Student’s t-test. (E)
Left: Representative traces of APV (50 μM) -induced blockade of whole-cell current of CA1 neurons in brain slices from control and chronically stressed mice. Scale bar = 40 pA, 1 min. Right: Histograms of the APV-induced blockade of whole-cell currents recorded from control (6 recordings, 3 rats) and chronically stressed mice (6 recordings, 3 rats). Mean ± SEM. *p < 0.05, Student’s t-test.