ABSTRACT
Conditioned fear is supported by a distributed network that prominently includes lateral and central amygdaloid nuclei. The role of corticomedial amygdaloid nuclei, including the medial nucleus (MeA), in fear acquisition or expression is not well understood. The present study demonstrates that pre-training excitotoxic lesions directed at the MeA disrupted both fear-potentiated startle (FPS) and conditioned freezing behavior elicited by re-exposure to a discrete olfactory cue. In contrast, such lesions had no effect on baseline startle reactivity or contextual FPS. These findings suggest that the MeA plays an obligatory role in either the acquisition or expression of olfactory conditioned fear, not limited by form of behavioral expression, but is not necessary for contextual conditioned fear.
