However, studies that have administered glucocorticoids alone to

However, studies that have administered glucocorticoids alone to animals prior to extinction training have found limited effects extinction learning performance (Barrett and Gonzalez-Lima, 2004 and Yang et al., 2006), suggesting more research is needed to fully characterize the effects of these hormones on within-session extinction training performance. Few studies have assessed the effects of acute

stress on extinction processes in humans. One investigation reported that using the cold-pressor task (CPT; a painful ice-water submersion www.selleckchem.com/products/lgk-974.html technique) before extinction training led to impairments in fear memory retrieval at the start of an extinction training session, a finding that was only seen in male participants (Bentz et al., 2013).

Due to both selleck chemicals the failure to retrieve the original fear association, and poor overall extinction performance, the effects of stress on extinction learning and retrieval, respectively, could not be assessed. Another study recently showed that male participants who were stressed using the CPT directly before a fear conditioning task displayed resistance to extinction training that followed (Antov et al., 2013). In animals, repeated or chronic stress consistently has been shown to impair extinction retention even after intact training (Miracle et al., 2006, Garcia et al., 2008 and Knox et al., 2012; Wilber et al., 2011). A recent study in rats showed that a single episode of acute stress induced directly before an extinction retention test led to retrieval deficits and the re-emergence of extinguished fear (Deschaux et al., 2013). Such retrieval deficits have been linked about to IL dysfunction since lesioning the IL region of the vmPFC in rodents has been shown to produce extinction retrieval deficits that are comparable to those seen after a stress induction (Farrell et al., 2010). Impairments in extinction retention have also been documented in animal populations bred for high trait-anxiety (Muigg et al., 2008). Stress hormones play a pivotal role in facilitating the consolidation of extinction

learning in both the amygdala and IL. For example, noradrenergic administration in the BLA facilitates extinction memory by boosting consolidation (Berlau and McGaugh, 2006). In the IL, direct infusions of propranolol before training impairs later extinction retrieval without affecting within-session performance, supporting the critical role of the IL in extinction retrieval. In contrast, propranolol administered directly into the IL after extinction training does not affect later retrieval, suggesting it leaves consolidation intact ( Mueller et al., 2008). This discrepancy is thought to be due to pre-training reductions in arousal, which may disrupt extinction learning by reducing the salience of conditioned stimuli, subsequently impairing consolidation.

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