Basolateral amygdala erk1/2 pathway underlie both the enhancement of anxiety-like behaviour and the facilitating influence on fear.

MALDONADO NM; ESPEJO PJ; MARTIJENA ID; MOLINA VA

Cancún

Encuentro; International Society for Neurochemistry and American Society for Neurochemistry 24th Biennial Joint Meeting.; 2013

International Society for Neurochemistry and American Society for Neurochemistry

It is well known that emotionally arousing experiences usually result in a robust and persistent memory trace and the expression of enhanced anxiety. Extensive data in humans and rodents have demonstrated that the stress effects on emotional processing and memory formation are largely mediated by the amygdala complex. It is well documented that the ERK pathway plays a major role in synaptic plasticity, learning and memory formation (Sweatt 2001; Thomas and Huganir 2004), and several reports indicated that ERK activation in amygdala after fear conditioning is require for fear memory consolidation (Schafe, Nadel et al. 1999; Schafe, Swank et al. 2008). In line with this evidence, recent "ndings showed a consistent enhancement of p-ERK expression in the BLA in the consolidation of contextual fear memory in stressed animals (Maldonado, Martijena et al. 2011). In addition, several studies reported that acute stress results in the activation of the ERK signaling cascade in brain regions that are essential components of the neural circuitry orchestrating environmental challenges-induced emotional responses (Ailing, Fan et al. 2008; Todorovic, Sherrin et al. 2009). Given the importance of the ERK cascade in stress effects and in the formation of fear memory, the present study investigated the potential involvement of the ERK pathway in amygdala subnuclei in the in!uence of a prior stressful event on the consolidation of a contextual fear memory and on the onset of anxiety-like behavior. A robust and persistent ERK2 activation was evident in the basolateral amygdala which lasts at least one day after the stressful experience. Moreover, such environmental challenge facilitated fear memory formation and increased anxiety-like behavior in the elevated plus maze. In addition, pretreatment with the intra-BLA infusion, but not into the central nucleus of the amygdala, with UO126 (MEK inhibitor), prevented the stressinduced facilitating influence on fear memory formation and anxiety-like behavior. Given that the activation of ERK1/2 pathway is essential for associative memory and for stress-induced emotional reactions, we propose that the activation of ERK2 in BLA following stress exposure is an important mechanism for the promoting influence of stress on both processes.