“Switch” protects against post-traumatic stress disorder

The newly discovered mechanism protects our brain from unbridled anxiety, informs Molecular Psychiatry.

Our brain has an extraordinary ability to adapt to changes in the environment, called plasticity by experts. Thanks to it, stress or trauma do not usually lead to mental disorders – although they sometimes develop, as in the case of post-traumatic stress disorder.

The team of Professor Robert Pawlak from the University of Exeter Medical School managed to identify the mechanism that protects against the development of uncontrolled anxiety. Scientists have shown that stressful events reprogram certain receptors in the amygdala, the emotional center of the brain. This, in turn, determines how the brain reacts to subsequent traumatic events.

These receptors (PAR1, i.e. receptors activated by protease) play a control role – under their influence, neurons inhibit or accelerate their activity.

Before the traumatic experience, PAR1 receptors usually keep the amygdala neurons active, arousing vivid emotions. However, after trauma, they inhibit the activity of the same neurons, inhibiting emotions and protecting against uncontrolled anxiety.

This helps not to overreact to apparent or insignificant threats – for example, a car accident victim does not need to be afraid of every car.

The team conducted studies on mice whose PAR1 receptors had been genetically disabled. The animals began to react even to weak unpleasant stimuli with pathological anxiety.

As noted by prof. Pawlak, the discovery that the same receptor can both excite and switch off neurons depending on previous experiences adds a whole new dimension to our knowledge of how the brain works and how emotions develop.

The authors of the study want to learn more about the above mechanism to find out whether the genetic defects of the PAR1 receptor are responsible for anxiety disorders and depression in some patients. This should lead to the development of new treatments in the future (PAP).

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