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Mental disorders
Sub-Topics
Depression and Manic Depression
Alzheimer’s-type Dementia

Linked
Help Human amygdala activation during conditioned fear acquisition and extinction: a mixed-trial fMRI study Differential prefrontal cortex and amygdalahabituation to repeatedly presentedemotional stimuli The Neurological Substrate Of Social Or Emotional Intelligence
Researcher
Mark G. Barad Mark G. Barad
Experiment
The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear Role of the Amygdala in Fear Extinction Measured with Potentiated Startle Context-Dependent Neuronal Activity in the Lateral Amygdala Represents Fear Memories after Extinction Neurons in medial prefrontal cortex signal memory for fear extinction
Memory for Extinction of Conditioned Fear Is Long-lasting and Persists Following Spontaneous Recovery Brain activity in ventromedial prefrontal cortexcorrelates with individual differences in negative affect Reversal of fear in the human brain
Original modules
Tool Module : Treating Anxiety Disorders Treating Anxiety Disorders
Experiment Module : Identifying the Brain Structures Involved in Conditioned Fear   Identifying the Brain Structures Involved in Conditioned Fear

In animal studies, researchers extinguish conditioned fears by ceasing to apply the aversive stimulus, thus teaching the animals that they no longer have anything to fear.

Suppose, for example, that researchers have conditioned a fear in a rat by letting it hear a certain sound, then applying an electrical shock to its paws through the floor of its metal cage. The rat soon learns to avoid the shock by jumping through a door into an adjacent compartment of the cage where the floor is not electrified. If the researchers then close the door and start playing the sound without applying the shock, the rat soon learns that the sound is no longer associated with the shock and stops trying to get through the door. The rat's avoidance behaviour is then said to have been extinguished.

This same process provides the basis for the cognitive-behavioural therapies that are used to treat anxiety disorders.

Link : Thérapies cognitivo-comportementales Research : John Watson
BRAIN ABNORMALITIES ASSOCIATED WITH ANXIETY DISORDERS

Conditioned fear (follow the Experiment module link to the left) is regarded as the primary mechanism underlying many anxiety disorders, such as phobias and post-traumatic stress disorder. A conditioned fear exists when a neutral stimulus is strongly associated with an aversive one in a person's mind. After a while, the neutral stimulus alone suffices to produce anxiety—for example, when the low rumble of thunder suddenly plunges a former soldier back into all the horrors of the battlefield.

Anxiety disorders can be treated successfully with behavioural therapies (see sidebar) that extinguish the underlying conditioned fears. This process of extinction involves gradually weakening the conditioned fear until the conditioned stimulus (in the preceding example, the sound of thunder) is no longer associated with the aversive stimulus (the horrors of battle). In other words, over time, the patient learns how to overcome the association that he or she had formed between a neutral stimulus and a fear. In addition to the passage of time, a change in context can also facilitate the extinction of a conditioned fear.  

Extinction is thus an adaptive phenomenon: if the actual threatening situation is not recurring, no purpose is served by continuing to experience fear simply because its context has recurred. Researchers have therefore proposed that certain anxiety disorders may be due to a malfunction in the mechanism by which conditioned fears are extinguished.

Also, a number of studies have shown that deconditioning through extinction does not involve actually erasing the conditioning, but rather learning something new in addition to it. Extinction is thus different from forgetting. The original fear is still there; it is simply masked and is no longer expressed.

  Other experimental data support the idea that fear conditioning and fear extinction are carried out by different parts of the brain. The role of the amygdala in fear conditioning is well established. The role of the prefrontal cortex in fear extinction is less well established, but the ventromedial portion of this cortex definitely plays a role in this process, just as it does in depression. This makes sense, because the prefrontal cortex has long been known to play a role in inhibiting inappropriate behavioural responses.

In experimental studies, when lesions were made in an animal's ventromedial prefrontal cortex, they did not prevent it from learning new conditioned fears. But when the researchers then attempted to extinguish a conditioned fear (for example, by subjecting the animal to a sound without the accompanying electric shock that it had previously been taught to expect), the process of extinction took much longer.

The precise role of the ventromedial prefrontal cortex remains ambiguous, however, because it does not seem to be needed to achieve the extinction itself, but only to recall the newly learned information some time after extinction has been achieved. These observations would therefore suggest that this structure's role is more to consolidate the extinction or to recall the context in which the extinction took place.

The ventromedial prefrontal cortex receives connections from the sensory areas and the amygdala and returns axons to the amygdala. It would therefore seem well placed to exercise cortical controls over the amygdala—for example, by generating the process of extinction. If these cortical controls are impaired, however, the extinction of a conditioned fear becomes very difficult. And indeed, one of the most classic symptoms of damage to the frontal lobes in human beings is the inability to cease a behaviour when it becomes inappropriate.

The prefrontal cortex also seems to participate, like the hippocampus, in the negative feedback loop that lowers the level of stress hormones when it becomes too high. And like the hippocampus, the prefrontal cortex might also become impaired by persistently high levels of glucocorticoids, thus interfering with this control mechanism and releasing the natural brake on the amygdala. Consequently, any new emotional stimulus would be more strongly encoded and would become very resistant to extinction.

Tool Module : Cybernetics

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