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The Journal of Neuroscience, August 10, 2005, 25(32):7429-7437; doi:10.1523/JNEUROSCI.2314-05.2005

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Behavioral/Systems/Cognitive
Prefrontal Control of the Amygdala

Ekaterina Likhtik, Joe Guillaume Pelletier, Rony Paz, and Denis Paré

Center for Molecular and Behavioral Neuroscience, Rutgers, The State University of New Jersey, Newark, New Jersey 07102

Accumulating evidence indicates that phobic and posttraumatic anxiety disorders likely result from a failure to extinguish fear memories. Extinction normally depends on a new learning that competes with the original fear memory and is driven by medial prefrontal cortex (mPFC) projections to the amygdala. Although mPFC stimulation was reported to inhibit the central medial (CEm) amygdala neurons that mediate fear responses via their brainstem and hypothalamic projections, it is unclear how this inhibition is generated. Because the mPFC has very sparse projections to CEm output neurons, the mPFC-evoked inhibition of the CEm is likely indirect. Thus, this study tested whether it resulted from a feedforward inhibition of basolateral amygdala (BLA) neurons that normally relay sensory inputs to the CEm. However, our results indicate that mPFC inputs excite rather than inhibit BLA neurons, implying that the inhibition of CEm cells is mediated by an active gating mechanism downstream of the BLA.

Key words: amygdala; medial prefrontal cortex; infralimbic; prelimbic; extinction; fear conditioning

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Received March 9, 2005; revised July 1, 2005; accepted July 1, 2005.

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