[4] 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).
[4] 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.
In this model, a neutral cue or context can come to elicit a conditioned response when it is paired with an unconditioned stimulus.
In this instance, a tone paired with a mild footshock can become a conditioned cue, eliciting a fear response when presented alone in the future.
As the animal learns that the cue or context no longer predicts the coming of the unconditioned stimulus, conditioned responding gradually decreases, or extinguishes.
In the operant conditioning paradigm, extinction refers to the process of no longer providing the reinforcement that has been maintaining a behavior.
[6] For example, a child who climbs under his desk, a response which has been reinforced by attention, is subsequently ignored until the attention-seeking behavior no longer occurs.
All that weekend I crossed streets with particular care and avoided all unnecessary risks to protect my discovery from loss through my accidental death.
Extinction can be a long process; therefore, it requires that the facilitator of the procedure be completely invested from beginning to end in order for the outcome to be successful.
This usually consists of a sudden and temporary increase in the response's frequency, followed by the eventual decline and extinction of the behavior targeted for elimination.
During its training history, every time the pigeon pecked the button, it will have received a small amount of bird seed as a reinforcer.
In perceptual control theory, the degree of output involved in any action is proportional to the discrepancy between the reference value (desired rate of reward in the operant paradigm) and the current input.
Extinction can increase these variations significantly as the subject attempts to acquire the reinforcement that previous behaviors produced.
Children with Autism Spectrum Disorder (ASD) are known to have restricted or repetitive behaviors that can cause problems when trying to function in day-to-day activities.
[11C] Raclopride is popular in studies focusing on striatal dopamine activity[21] and ease of use considering a shorter half-life (about 20 minutes).
Additionally, simultaneous PET and fMRI allow researchers to capture both dopamine binding potential and blood oxygen level-dependent (BOLD) signals during the task.
Recent studies highlight the critical role of dorsolateral and ventromedial prefrontal cortex regions (vmPFC), together with other areas like the anterior insula, amygdala, and hippocampus in facilitating fear extinction processes.
[25] D-Cycloserine (DCS) is a partial agonist for the glutamate receptor NMDA at the glycine site, and has been trialed as an adjunct to conventional exposure-based treatments based on the principle of cue extinction.
[4] The posterior cingulate cortex (PCC) and temporoparietal junction (TPJ) have also been identified as regions that may be associated with impaired extinction in adolescents.
During infancy and childhood, learning extinction is especially persistent, which some have interpreted as erasure of the original CS-US association,[40][41][42] but this remains contentious.
In contrast, during adolescence and adulthood extinction is less persistent, which is interpreted as new learning of a CS-no US association that exists in tandem and opposition to the original CS-US memory.