Hypothetical model for impaired extinction and extinction fear memory after mild TBI (mTBI). Layer II/III pyramidal neurons in the IL receive information regarding the context via projections from limbic structures (e.g., amygdala, hippocampus, entorhinal cortex, and cingulate cortex) which synapse on their dendrites. In addition, these neurons also receive thalamic input predominately on their proximal dendrites. A reduction in spine density of these neurons as a result of mTBI is likely decrease the ability of these neurons to initiate action potentials. This reduction in firing rate will decrease the ability of the IL to directly or indirectly stimulate the inhibitory GABAergic neurons in the intercalated cells of the amygdala (ITC). As a result, the output from the CeA is expected to remain elevated, leading to physical manifestations of fear (e.g., heart rate, freezing behavior, and stress hormones). This model also predicts that reduced activity in layer II/III neurons will decrease the output from layer V/VI neurons. BLA, basolateral amygdala; CeA, central nucleus of the amygdala; CG, central gray; IL, infralimbic cortex; LH, lateral hypothalamus; PVN, paraventricular nucleus.