Fig. 2.

NE has no direct effect on baseline glutamatergic synaptic transmission in thalamo-amygdala pathway. (A) Values of amplitude of the NMDA receptor-mediated EPSCs (normalized by the pre-NE baseline) are plotted as a function of time (mean ± SEM; n = 10 neurons). Solid bar shows the duration of 10 μM NE application. Traces (top) show NMDAR EPSCs recorded before (1) and during (2) NE application. Synaptic currents were recorded in the presence of the AMPAR antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 μM) and PTX (50 μM) at a holding potential of +30 mV. (B) Current-voltage plot of the NMDA receptor EPSCs. Synaptic currents (Inset) were recorded in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione and PTX at holding potentials of −70 mV to +50 mV under baseline conditions (filled symbols) and ≈15 min after switching to the NE-containing solution (open symbols; n = 6 neurons). Traces are averages of three EPSCs recorded at each holding potential. (C) The AMPAR-mediated thalamo-amygdala EPSCs were recorded from pyramidal neurons at a holding potential of −70 mV (n = 6 neurons). Solid bar shows the duration of 10 μM NE application. Traces (top) are averages of three EPSCs recorded before (1) and during (2) NE application. (D) Application of NE induced potentiation of the thalamo-amygdala EPSC when α₂-adrenoreceptors were blocked by yohimbine (20 μM; n = 5). This potentiation was reversed by 10 μM propranolol. (E) NE application produced depression of the EPSC when β-adrenoreceptors were blocked by propranolol (10 μM; n = 4). Yohimbine partially blocked this potentiation. (F) Summary plot of the effects of NE on glutamatergic EPSCs in thalamic input to the LA. Error bars indicate SEM. (G) Responses of LA neurons to prolonged current injections (500 ms, 200 pA) recorded before (control) and during NE application. (H) Summary plots of the experiments as in G (n = 8; mean ± SEM).