Extinction (psychology)

Extinction is observed in both operantly conditioned and classically conditioned behavior. When operant behavior that has been previously reinforced no longer produces reinforcing consequences the behavior gradually stops occurring. In classical conditioning, when a conditioned stimulus is presented alone, so that it no longer predicts the coming of the unconditioned stimulus, conditioned responding gradually stops. For example, after Pavlov's dog was conditioned to salivate at the sound of a metronome, it eventually stopped salivating to the metronome after the metronome had been sounded repeatedly but no food came. Many anxiety disorders such as posttraumatic stress disorder are believed to reflect, at least in part, a failure to extinguish conditioned fear.

The dominant account of extinction involves associative models. However, there is debate over whether extinction involves simply "unlearning" the unconditional stimulus (US) – Conditional stimulus (CS) association (e.g., the Rescorla–Wagner account) or, alternatively, a "new learning" of an inhibitory association that masks the original excitatory association (e.g., Konorski, Pearce and Hall account). A third account concerns non-associative mechanisms such as habituation, modulation and response fatigue. Myers and Davis laboratory work with fear extinction in rodents has suggested that multiple mechanisms may be at work depending on the timing and circumstances in which the extinction occurs.

Given the competing views and difficult observations for the various accounts researchers have turned to investigations at the cellular level (most often in rodents) to tease apart the specific brain mechanisms of extinction, in particular the role of the brain structures (amygdala, hippocampus, the prefrontal cortex), and specific neurotransmitter systems (e.g., GABA, NMDA). A recent study in rodents by Amano, Unal and Paré published in Nature Neuroscience found that extinction of a conditioned fear response is correlated with synaptic inhibition in the fear output neurons of the central amygdala that project to the periaqueductal gray that controls freezing behavior. They infer that inhibition derives from the ventromedial prefrontal cortex and suggest promising targets at the cellular level for new treatments of anxiety.

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