Current findings help reconcile the contradictory reports regarding the role of infralimbic cortex in the environmental control of appetitive behavior.

The prelimbic and infralimbic prefrontal cortex (PFC) process distinct inputs from rostral and caudal basolateral amygdala (BLA), which engage different populations of projection neurons, via both direct connections and polysynaptic activity within the local network.

Prefrontal dopamine regulates inhibition of fear extinction circuits in the infralimbic cortex and disinhibition of fear expression circuits in the amygdala, leading to fear reinstatement.

Insulin-like growth factor-1 activates the prefrontal cortex and improves the extinction of aversive memories.

Extinction and overexpectation lead to the same behavioural outcome, that is, reduction in learned fear, but engage different cortical areas.

Behavior- or optogenetic-driven activation of a basolateral amygdala projection to the nucleus accumbens enhances infralimbic cortex activity and long-term fear extinction.

Endocannabinoids modulate ventral hippocampal inputs to the infralimbic prefrontal cortex by dampening feed-forward inhibition mediated by cholecystokinin-expressing (CCK+) interneurons onto layer 5 intratelencephalic (IT) cells.

A neural circuit between the prefrontal cortex and bed nucleus of the stria terminalis is shown to limit fear to cues that only partially associate with threat.

aIC to mPFC connections are correlative and necessary both for taste novelty behavior and learning while the reciprocal connection from mPFC to aIC is correlative and necessary for novelty behavior.

Social defeat stress induces transcription factor Npas4 expression in the medial prefrontal cortex and its chronic stress-induced changes in excitatory synaptic transmission, reduction of dendritic spine density, and anhedonia-like behaviors.