ERK1/2 pathway underlie both the enhancement of anxiety-like behavior and the facilitationg influence on fear memory following stress

NOELIA MARTINA MALDONADO; IRENE DELIA MARTIJENA; VÍCTOR ALEJANDRO MOLINA

Congreso; XXVI Congreso Anual de la Sociedad Argentina De Investigación En Neurociencia; 2011

Exposure to emotionally arousing experiences elicits a robust and persistent memory and enhancesanxiety. The amygdala complex plays a key role in stress-induced emotional processing and in thefear memory formation. It is well known that ERK activation in the amygdala is a prerequisite forfear memory consolidation. Moreover, stress elevates p-ERK2 levels in several areas of the brainstress circuitry. Therefore, given that the ERK1/2 cascade is activated following stress and that therole of this cascade is critical in the formation of fear memory, the present study investigated thepotential involvement of p-ERK2 in amygdala subnuclei in the promoting influence of stress on fearmemory formation and on anxiety-like behavior. A robust and persistent ERK2 activation was notedin the Basolateral amygdala (BLA), which was evident at 5 min after restraint and lasted at leastone day after the stressful experience. Midazolam, a short-acting benzodiazepine ligand,administered prior to stress prevented the increase in the p-ERK2 level in the BLA. Pretreatmentwith intra-BLA infusion of U0126 (MEK inhibitor), but not into the adjacent central nucleus of theamygdala, attenuated the stress-induced promoting influence on fear memory formation. Finally,U0126 intra-BLA infusion prevented the enhancement of anxiety-like behavior in stressed animals.These findings suggest that the selective ERK2 activation in BLA following stress exposure is animportant mechanism for the occurrence of the promoting influence of stress on fear memory andon anxiety-like behavior