Effects of corticosterone and the β‐agonist isoproterenol on glutamate receptor‐mediated synaptic currents in the rat basolateral amygdala

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 μ m 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 μ m ), 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 μ m 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.