β-Adrenergic facilitation of synaptic plasticity in the rat basolateral amygdala in vitro is gradually reversed by corticosterone

Abstract

The rat basolateral amygdala is important for emotional learning; this is modulated by noradrenaline and corticosterone. We report that the β-adrenergic agonist isoproterenol markedly enhances synaptic plasticity induced in the basolateral amygdala by a weak stimulation paradigm but is ineffective with stronger protocols. Simultaneous application of corticosterone gradually reversed the facilitatory effect of isoproterenol. When corticosterone was briefly applied several hours prior to isoproterenol, facilitatory effects of the β-agonist were entirely suppressed. This suggests that in the basolateral amygdala, β-adrenergic influences promote synaptic plasticity; this is gradually normalized by corticosterone, preventing the network from overshooting.