The decline of GluR1-containing AMPARs at axo-shaft synapses with unpaired training does not seem consistent with a cellular mechanism for either context conditioning or conditioned inhibition. However, this change is consistent with a nonassociative sensitization process resulting from US exposure. A variety of stressors can lead to hyperexcitability in the amygdala, often manifested as impairments in local γ-aminobutyric acid (GABA)ergic inhibition (Braga et al., 2004; Rainnie et al., 2004; Rodriguez Manzanares et al., 2005). Thus, USs that are not predicted by any explicit CS may prime the amygdala for future associative conditioning and/or lower the threshold for amygdala activation by other fear-eliciting stimuli. Recent studies indicate that suppression of feed-forward inhibition is important for induction of LTP in the LA (Bissiere et al., 2003; Kodirov et al., 2006), consistent with this priming hypothesis.
