Fig. 5: ELA impairs glutamatergic transmission and reduces the expression of GluR1 and NR1 subunits.
A, B Input-output curves of AMPAR-EPSC and NMDAR-EPSC in response to a series of stimuli in ELA mice versus controls. ELA mice exhibited a reduced EPSC when the stimulation was performed at 7V and 9V (F1,14 = 420.1 and 78.41 for AMPAR- and NMDAR-EPSC, respectively, P < 0.0001; post hoc test, **P < 0.01). Representative EPSC traces are presented on right panels. The clamped cells were depolarized to +60 mV to record NMDAR-EPSC. Scale bars = 30 pA, 20 ms (A) and 30 pA, 100 ms (B). C, D Miniature EPSC (mEPSC) amplitude and frequency were measured in layers II-III and V-VI of the PrL. Decreased mEPSC was apparent in ELA mice versus controls (F1,28 = 69.99 and 44.28 for the amplitude and frequency, respectively; post hoc test, **P < 0.01). E–G The protein levels of AMPAR (GluR1 and GluR2) and NMDAR (NR1, NR2A, and NR2B) subunits in the PrL of ELA mice versus controls. The optical densities of bands corresponding to the subunits were normalized to respective actin levels and expressed as a percentage of the controls. Decreased expressions of GluR1 (F1,14 = 170.1, P < 0.0001; post hoc test, **P < 0.01) and NR1 (F1,14 = 9.186, P = 0.009; post hoc test, **P < 0.01) were observed in ELA mice (G).
