EN
INTRODUCTION: In the ventral tegmental area (VTA), norepinephrine (NA) promotes phasic dopamine (DA) release in the forebrain, thus regulating conditioned behaviors, such as fear conditioning. We recently demonstrated that α2-AR blockade in the VTA reduces DA release in the mesolimbic but not mesocortical pathway. Under the influence of stress, downregulation of α2-AR occurs in stria terminalis, therefore we hypothesize that the mechanism in VTA is similar. The net effect of α2-AR signaling on DA release may depend on the plasticity related to factors such as acute stress. AIM(S): The aim of this study is to demonstrate the impact of acute stress on the ability of α2-AR signalling in stressed versus naïve, non-stressed, rats to modulate phasic DA release in the basolateral amygdala (BLA). METHOD(S): For the study of dopaminergic signaling, fast-scan cyclic voltammetry was used in urethane anesthetized rats. The stimulation electrode, together with the guide cannula, was placed in the VTA, while the recording carbon‑fiber microelectode in BLA. In the case of stressed rats, animals were subjected to fear conditioning (0.9‑mA electric footshock) 24 hours before FSCV. RESULTS: Intra‑VTA administration of the α2-AR selective antagonist RX‑821002 strongly reduced phasic DA release in the BLA in naïve rats. In contrast, only modest attenuation of DA by RX‑821002 was observed in the BLA of stressed animals. CONCLUSIONS: Our results are consistent with the idea that α2-AR signalling in various structures undergoing NAergic modulation is subject to plasticity related to stress. Here, we show that an acute stressful stimulus is sufficient to elicit this form of plasticity, potentially via α2‑AR downregulation.