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

MALDONADO, N.M; ESPEJO, P.J.; IRENE DELIA MARTIJENA; VICTOR ALEJANDRO MOLINA

Congreso; 24 ISN-ASN Biennial Meeting; 2013

American Society for Neurochemistry (ASN)

It is well known that emotionally arousing experiences usually result in a robust and persistentmemory trace and the expression of enhanced anxiety. Extensive data in humans and rodentshave demonstrated that the stress effects on emotional processing and memory formation arelargely mediated by the amygdala complex. It is well documented that the ERK pathway plays amajor role in synaptic plasticity, learning and memory formation (Sweatt 2001; Thomas andHuganir 2004), and several reports indicated that ERK activation in amygdala after fearconditioning is required for fear memory consolidation (Schafe, Nadel et al. 1999; Schafe, Swanket al. 2008). In line with these evidence, recent findings showed a consistent enhancement of pERK 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 theactivation of the ERK signaling cascade in brain regions that are essential components of theneural circuitry orchestrating environmental challenges induced emotional responses (Ailing, Fanet al. 2008; Todorovic, Sherrin et al. 2009). Given the importance of the ERK cascade in stresseffects and in the formation of fear memory, the present study investigated the potentialinvolvement of the ERK pathway in amygdala subnuclei in the influence of a prior stressful eventon the consolidation of a contextual fear memory and on the onset of anxiety-like behavior. Arobust and persistent ERK2 activation was evident in the basolateral amygdala which lasts atleast one day after the stressful experience. Moreover, such environmental challenge facilitatedfear memory formation and increased anxiety-like behavior in the elevated plus maze. Inaddition, pretreatment with the intra-BLA infusion, but not into the central nucleus of theamygdala, with UO126 (MEK inhibitor), prevented the stress induced facilitating influence onfear memory formation and anxiety-like behavior. Given that the activation of ERK1/2 pathway isessential for associative memory and for stress-induced emotional reactions, we propose thatthe activation of ERK2 in BLA following stress exposure is an important mechanism for thepromoting influence of stress on both processes .