Behavioral and field potential studies suggest that – shortly after stress – noradrenaline and corticosterone interact to affect the function of basolateral amygdala (BLA) neurons. Here, we tested, at the single-cell level, to what extent α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) receptor-mediated and N-methyl-d-aspartate (NMDA) receptor-mediated synaptic responses of identified BLA neurons are affected by relatively low concentrations of the β-agonist isoproterenol, how this is influenced by concomitant application of corticosterone, and how isoproterenol effects are influenced by corticosterone given several hours in advance. We observed that isoproterenol concentration-dependently enhances AMPA receptor-mediated (but not NMDA receptor-mediated) responses; near-maximal effects were induced by 1 μm isoproterenol. Corticosterone alone did not rapidly affect AMPA and NMDA-mediated responses. NMDA-mediated responses were also not affected by the hormone in a delayed manner; AMPA-mediated responses were slowly suppressed by corticosterone, but only with high stimulation intensities. If corticosterone was co-applied with isoproterenol (0.4 or 1 μm), facilitation of AMPA-mediated responses was comparable to that seen with isoproterenol alone. However, if corticosterone was applied several hours in advance of the β-agonist, the effect of 0.4 μm isoproterenol on AMPA-mediated responses was reduced. This supports the notion that, in the BLA, isoproterenol facilitates synaptic transmission, a process that can be suppressed by corticosterone in a slow manner. Overall, the data suggest that, despite the previously reported ability of corticosterone to cause long-term increases in excitability in the BLA, the hormone still retains some capacity to slowly exert a normalizing action on local activity.