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. Author manuscript; available in PMC: 2018 Sep 21.
Published in final edited form as: Nat Rev Neurosci. 2018 Sep;19(9):535–551. doi: 10.1038/s41583-018-0039-7

Fig. 3|. Amygdala microcircuits implicated in fear conditioning.

Fig. 3|

The schematic offers a simplified representation of the mouse amygdala microcircuits that are currently implicated in fear conditioning. During fear conditioning, output neurons from the central amygdala increase their responsiveness to a conditioned stimulus. This increased responsiveness is likely to occur through the mutual interaction of two parallel ‘fear on’ and ‘fear off’ pathways that project to these neurons from the basolateral amygdala (BLA) and lateral amygdala (LA). There is an additional pathway for the establishment of competing fear extinction memories that is likely to originate from neurons in the infralimbic cortex that activate intercalated cells in the amygdala (‘fear ext.’ neurons). Although our understanding of these pathways remains incomplete, several cell types have been demonstrated to modify the expression of fear behaviours. Excitatory connections are indicated with arrows. Inhibitory connections are indicated with blunt arrows. Solid lines designate proven connections, whereas dashed lines illustrate hypothetical connections. CeL, lateral division of the central amygdala; CeM, medial division of the central amygdala; CRH, corticotropin-releasing hormone; FOXP2, forkhead box protein P2; GRP, gastrin-releasing peptide; ITCd, ITCv and ITCl, intercalated cell masses dorsal, ventral and lateral, respectively; PRKCD, protein kinase C delta type; PV, parvalbumin; SST, somatostatin; TAC2, protachykinin 1 (also known as TAC1); THY1, Thy-1 membrane glycoprotein.