Extinction occurs when a previously reinforced response is no longer reinforced (operant) or when a conditioned stimulus is repeatedly presented without the unconditioned stimulus (classical). The conditioned behavior gradually diminishes. However, a critical modern insight is that extinction does not erase the original learning — it creates new, inhibitory learning that competes with the original association. Multiple phenomena demonstrate that the original learning survives extinction.
Evidence That Original Learning Survives
Spontaneous recovery: the extinguished response returns after a rest period. Renewal: the extinguished response returns when tested in a context different from the extinction context. Reinstatement: the extinguished response returns after unsignaled presentations of the US. Rapid reacquisition: relearning after extinction is faster than original learning. These phenomena collectively demonstrate that extinction creates a new association (CS-no US) that is context-dependent, while the original association (CS-US) remains intact.
Extinction is the theoretical basis for exposure therapy, the most effective behavioral treatment for anxiety disorders and phobias. By repeatedly presenting the feared stimulus (CS) without the aversive outcome (US), the fear response is gradually reduced. Understanding that extinction is context-dependent has improved therapy: conducting exposure in multiple contexts, including the context where fear occurs naturally, helps prevent the return of fear (renewal) outside the therapy setting.
Neural Mechanisms
The prefrontal cortex — particularly the ventromedial prefrontal cortex (vmPFC) or infralimbic cortex in rodents — plays a critical role in extinction learning. During extinction, the vmPFC develops inhibitory connections to the amygdala, suppressing the fear response. The hippocampus provides contextual information that determines whether the original fear memory or the extinction memory is expressed. Impaired extinction learning, involving dysfunctional prefrontal-amygdala circuits, is implicated in anxiety disorders and PTSD.