In:
eLife, eLife Sciences Publications, Ltd, Vol. 4 ( 2015-07-30)
Abstract:
Anxiety disorders affect millions of people worldwide. While many people with anxiety disorders can recover with appropriate treatment, about 40% of these individuals will encounter a relapse of their condition. Researchers can investigate the causes of relapses by creating animal models of the processes involved. For example, if a mouse receives a small shock every time it enters a particular cage, it will learn to associate that cage with the shock. Once this association has been created, it can be ‘undone’ using a procedure called extinction. In the cage example, this may be performed by placing the mouse in the cage for a long time, but without giving it any shocks. Over time, the animal learns that the cage is no longer linked to an unpleasant outcome. However, if a mouse is given a reminder shock after extinction has occurred, the original association between the cage and the shock is re-established. This is known as fear reinstatement and is similar to a relapse. A number of brain regions are thought to be involved in fear reinstatement. One such region, the amygdala, is heavily involved in fear responses. It is thought that another part of the brain, the medial prefrontal cortex (mPFC), can suppress the amygdala's responses, consequently reducing the animal's anxiety. While we have a good idea of which parts of the brain are involved in fear processing, we don't yet know how they work together to create a relapse. Hitora-Imamura et al. used the aforementioned method of selectively giving mice small shocks when they entered cages to induce fear, extinction, and fear reinstatement and examined how this affected the mice's brain activity. As expected, fear could be linked to activity in the amygdala. During extinction, high levels of activity in the medial prefrontal cortex suppressed the amygdala's response. When the mice experienced the reminder shock, a chemical called dopamine was released. When dopamine entered the medial prefrontal cortex, the region's activity was reduced, removing the ‘brakes’ from the amygdala and reinstating the mice's fear. The finding that dopamine is involved in fear reinstatement is particularly important, as many commonly abused drugs are known to increase levels of dopamine in the brain. Dopamine's role in fear reinstatement may explain why substance abuse is so closely linked to anxiety disorders.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.08274.001
DOI:
10.7554/eLife.08274.002
DOI:
10.7554/eLife.08274.003
DOI:
10.7554/eLife.08274.004
DOI:
10.7554/eLife.08274.005
DOI:
10.7554/eLife.08274.006
DOI:
10.7554/eLife.08274.007
DOI:
10.7554/eLife.08274.008
DOI:
10.7554/eLife.08274.009
DOI:
10.7554/eLife.08274.010
DOI:
10.7554/eLife.08274.011
DOI:
10.7554/eLife.08274.012
DOI:
10.7554/eLife.08274.013
DOI:
10.7554/eLife.08274.014
DOI:
10.7554/eLife.08274.015
DOI:
10.7554/eLife.08274.016
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2015
detail.hit.zdb_id:
2687154-3
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