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Brief exposure to predator odor and resultant anxiety enhances mesocorticolimbic activity and enkephalin expression in CD‐1 mice

The present study assessed alterations in mesolimbic enkephalin (ENK) mRNA levels after predator [2,5‐dihydro‐2,4,5‐trimethylethiazoline (TMT)] and non‐predator (butyric acid) odor encounter and/or light–dark (LD) testing in CD‐1 mice immediately, 24, 48 and 168 h after the initial odor encounter and/or LD testing. The nucleus accumbens, ventral tegmental area, basolateral (BLA), central (CEA) and medial amygdaloid nuclei, prelimbic and infralimbic cortex were assessed for fos‐related antigen (FRA) and/or ENK mRNA as well as neuronal activation of ENK neurons (FRA/ENK). Mice exposed to TMT displayed enhanced freezing and spent less time in the light of the immediate LD test relative to saline‐ or butyric acid‐treated mice. Among mice exposed to TMT, LD anxiety‐like behavior was associated with increased FRA in the prelimbic cortex and accumbal shell and decreased ENK‐positive neurons in the accumbal core. Mice displaying high TMT‐induced LD anxiety exhibited increased ENK‐positive neurons in the BLA, CEA and medial amygdaloid nuclei relative to mice that displayed low anxiety‐like behavior in the LD test after TMT exposure. In the BLA and CEA, ‘high‐anxiety’ mice also displayed increased FRA/ENK after TMT exposure and LD testing. In contrast to neural cell counts, the level of ENK transcript was decreased in the BLA and CEA of ‘high‐anxiety’ mice after TMT exposure and LD testing. These data suggest that increased FRA may regulate stressor‐responsive genes and mediate long‐term behavioral changes. Indeed, increased ENK availability in mesolimbic sites may promote behavioral responses that detract from the aversiveness of the stressor experience.