September 24, 2003 | Gregory J. Quirk, Ekaterina Likhtik, Joe Guillaume Pelletier, and Denis Paré
Stimulation of the medial prefrontal cortex (mPFC) reduces the responsiveness of central amygdala (Ce) output neurons to inputs from the insular cortex and basolateral amygdala (BLA). This study demonstrates that mPFC stimulation inhibits the transmission of fear-related signals from the BLA to the Ce, which is critical for the expression of conditioned fear. The mPFC projects to the Ce and may exert feedforward inhibition on Ce output neurons, thereby reducing the expression of fear responses. The findings support the idea that the mPFC gates the transmission of fear signals from the BLA to the Ce, possibly through GABAergic intercalated cells. This inhibition is effective in both rats and cats, suggesting that the mPFC plays a key role in the extinction of conditioned fear by modulating amygdala output. The study highlights the importance of the mPFC in the storage and expression of extinction memory, as well as its role in inhibiting fear responses through direct projections to the Ce and other brainstem and hypothalamic targets. The results provide direct physiological evidence for the mPFC's role in reducing fear responses by inhibiting amygdala output.Stimulation of the medial prefrontal cortex (mPFC) reduces the responsiveness of central amygdala (Ce) output neurons to inputs from the insular cortex and basolateral amygdala (BLA). This study demonstrates that mPFC stimulation inhibits the transmission of fear-related signals from the BLA to the Ce, which is critical for the expression of conditioned fear. The mPFC projects to the Ce and may exert feedforward inhibition on Ce output neurons, thereby reducing the expression of fear responses. The findings support the idea that the mPFC gates the transmission of fear signals from the BLA to the Ce, possibly through GABAergic intercalated cells. This inhibition is effective in both rats and cats, suggesting that the mPFC plays a key role in the extinction of conditioned fear by modulating amygdala output. The study highlights the importance of the mPFC in the storage and expression of extinction memory, as well as its role in inhibiting fear responses through direct projections to the Ce and other brainstem and hypothalamic targets. The results provide direct physiological evidence for the mPFC's role in reducing fear responses by inhibiting amygdala output.