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. Author manuscript; available in PMC: 2020 Apr 3.
Published in final edited form as: Neuron. 2019 Apr 3;102(1):60–74. doi: 10.1016/j.neuron.2019.03.017

Figure 2. A simplified schematic of the neural threat circuitry.

Figure 2.

The amygdala and its subnuclei are key nodes of threat and trauma-relevant encoding. The lateral amygdala (LA) and the lateral central amygdala (CEA-l) receive input from sensory cortices and thalamic structures (Thal) and represent a major site of threat-related neuronal plasticity. This plasticity is controlled by reciprocal connections between the basal amygdala (BA) and the prelimbic cortex (PL) as well as between the BA and the ventral hippocampus (vHC). Subsequently, the medial part of the central amygdala (CEA-m) projects to the hypothalamus (HYP) and other subcortical and brainstem regions to promote threat. Threat extinction is controlled by different circuits within the same structures. Input from the infralimbic cortex (IL) to the BA and to the intercalated (ITC) cells of the amygdala is crucial in reducing threat output from central amygdala nuclei (CE) to the hypothalamus (HYP) and the periaqueductal grey (PAG).