Abstract
The amygdala plays an important role in the responses to predator threat. Glutamatergic processes in amygdala regulate the behavioral responses to predator stress, and we have found that exposure to ferret odor activates glutamatergic neurons of the basolateral amygdala [BLA] which are known to project to the central amygdala [CeA]. Therefore, we tested if predator stress would increase glutamate release in the rat CeA using in vivo microdialysis, while monitoring behavioral responses during a 1 h exposure to ferret odor. Since injections of mu opioid receptor [MOR] agonists and antagonists into the CeA modulate behavioral responses to predator odor, we locally infused the MOR agonist DAMGO or the MOR antagonist CTAP into the CeA during predator stress to examine effects on glutamate efflux and behavior. We found that ferret odor exposure increased glutamate, but not GABA, efflux in the CeA, and this effect was attenuated by tetrodotoxin. Interestingly, increases in glutamate efflux elicited by ferret odor exposure were blocked by infusion of CTAP, but CTAP did not alter the behavioral responses during predator stress. DAMGO alone enhanced glutamate efflux, but did not modulate glutamate efflux during predator stress. These studies demonstrate that ferret odor exposure, like other stressors, enhances glutamate efflux in the CeA. Further, they suggest that activation of MOR in the CeA may help shape the defensive response to predator odor and other threats.