Noradrenergic-glucocorticoid mechanisms in emotion-induced amnesia: from adaptation to disease

Discussions The interaction of emotion and episodic encoding has costs and benefits. These costs and benefits have been characterized in oddball experiments, where a violation of prevailing neutral context through aversive oddballs is associated with subsequent hypermnesia for the aversive oddball and peri-emotional amnesia for the neutral context. Both hypermnesia and peri-emotional amnesia are amygdala-dependent and vary as a function of noradrenergic-glucocorticoid input to the amygdala during emotional episodic encoding. Pharmacological enhancement of this input allows to model the maladaptive effects of emotion on episodic encoding. Extrapolation of these findings to conditions of emotional trauma suggests that disinhibited noradrenergic-glucocorticoid signaling could serve as a crucial etiological contributor to the pathogenesis of peri-traumatic amnesia (PTA) and post-traumatic stress disorder (PTSD). Conclusions Immediate pharmacological blockade of noradrenergic-glucocorticoid signaling might prove effective in the secondary prevention of PTA and PTSD.