Trace fear conditioning is used to study these mechanisms by inserting a trace interval between the end of the CS and the beginning of the US. However, CS and US do not necessarily occur simultaneously in nature, and the brain has evolved mechanisms to associate temporally distinct events.
Canonical delay fear conditioning is performed by terminating the CS and US at the same time. The CS-US pair elicits fear behaviors, including freezing and fleeing, which are often species-specific. Fear conditioning is widely used to study this association and is performed by pairing a neutral stimulus (conditioned stimulus, CS), such as a tone, with a punishing stimulus (unconditioned stimulus, US), such as a shock ( Estes and Skinner, 1941). Learning to associate environmental cues with subsequent adverse events is an important survival skill. The neural plasticity in the LA leads to trace fear memory formation. In summary, high-frequency activation of EC neurons triggers the release of CCK in their projection terminals in the LA, potentiating auditory response in LA neurons. We discovered that CCK-positive neurons project from the EC to the lateral nuclei of the amygdala (LA), and inhibition of CCK-dependent signaling in the EC prevented long-term potentiation of the auditory response in the LA and formation of trace fear memory. We adopted both loss-of-function and gain-of-function experiments to demonstrate that release of the cholecystokinin (CCK) from the EC is required for trace fear memory formation. We identified the entorhinal cortex (EC) as a critical component of sensory signaling to the amygdala. Here, we utilized trace fear conditioning to study the formation of trace fear memory in mice. Although fear memory formation is essential for survival and fear-related mental disorders, the neural circuitry and mechanism are incompletely understood.
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