Although more research is required to understand the effects of stress on avoidance strategies, avoidant behaviors are common among anxiety patients (Eifert and Forsyth, 2007, Craske and Barlow, 1988 and Sprang and LaJoie, 2009), suggesting that stress may enhance well-practiced avoidance strategies. It should be noted that although avoiding an aversive outcome may attenuate fear responses, the habitual avoidance of fearful situations may also prevent one from confronting aversive stimuli Z-VAD-FMK price and engaging in extinction processes, which can be detrimental to the treatment of anxiety symptoms. Therefore, while stress may hinder the initiation of avoidance behavior

during learning, overuse of avoidance

strategies may lead to habitual, potentially maladaptive avoidance behaviors that are facilitated by stress. Since the fear regulation techniques discussed above can be vulnerable see more to the effects of acute stress, as well as other contextual and temporal factors, emerging research in animals and humans has examined the interference or blockade of fear memory reconsolidation as a putative alternative to change fear. Normative models of memory suggest that immediately after learning, there is window of time in which newly encoded information is susceptible to interference. However, recent research suggests that memories must undergo an additional phase of consolidation each time they are reactivated, a restabilization process referred to as reconsolidation. Since it is often not feasible to interfere with the initial consolidation ADP ribosylation factor of traumatic experiences, interfering with reconsolidation offers the possibility of altering traumatic memories in a more permanent manner. In a typical reconsolidation paradigm, after an aversive association is acquired and consolidated, a time-dependent reconsolidation window is induced by a single presentation of the CS to reactivate the aversive memory. A variety of behavioral or pharmacological manipulations

can then be used during the presumed reconsolidation window to alter memory re-storage before later testing for the conditioned responses in the presence of the CS. Research in humans (Schiller et al., 2010, Schiller et al., 2014 and Steinfurth et al., 2014; see Schiller and Phelps, 2011 for review) and animals (Nader et al., 2000, Monfils et al., 2009, Einarsson and Nader, 2012 and Hong et al., 2013) has now demonstrated that disrupting or interfering with reconsolidation leads to the persistent modification of amygdala-dependent aversive associations. Recent research in rodents suggests that interfering with the reconsolidation of aversive association induces plasticity in the LA (Monfils et al., 2009 and Clem and Huganir, 2010) and in humans, reconsolidation of fear memory leads to diminished BOLD responses in the amygdala (Agren et al.