Why anxiety doesn’t go away in some

Washington -  Researchers have decoded a molecular mechanism that sheds light on how trauma can become engraved in the brain.

Feelings of anxiety very effectively prevent people from getting into situations that are too dangerous.

Those who have had a terrible experience initially tend to avoid the place of tragedy out of fear. If no other oppressive situation arises, normally the symptoms of fear gradually subside.

“The memory of the terrible events is not just erased,” Dr. Andras Bilkei Gorzo, first author of the study from the Institute for Molecular Psychiatry at the University of Bonn, said.

“Those impacted learn rather via an active learning process that they no longer need to be afraid because the danger has passed,” Bilkei said.

But following extreme psychical stress resulting from wars, hostage-takings, accidents or catastrophes chronic anxiety disorders can develop which even after months don’t subside.

Scientists in the fields of psychiatry, molecular psychiatry and radiology at the University of Bonn are all involved in probing into why is it that in some people terrible events are deeply

engraved in their memory, while after a while others seem to have completely put aside any anxiety related to the incident.

“We were able to demonstrate by way of a series of experiments that dynorphin plays an important role in weakening anxiety,” Andreas Zimmer, Director of the Institute for Molecular

Psychiatry at the University of Bonn, said.

The substance group in question is opiods which also includes, for instance, endorphins. The latter are released by the body of athletes and have an analgesic and euphoric effect. The

reverse, however, is true of dynorphins: They are known for putting a damper on emotional moods.

The team of researchers working with Zimmer tested the exact impact of dynorphins on the brain using mice whose gene for the formation of this substance had been disabled.

After being exposed to a brief and unpleasant electric shock, the animals exhibited persistent anxiety symptoms, even if they hadn’t been confronted with the negative stimulus over a longer

time.

Mice exhibiting a normal amount of released dynorphin were anxious to begin with as well, but the symptoms quickly subsided.

Next they showed that these results can be transferred to people.

“We took advantage of the fact that people exhibit natural variations of the dynorphin gene that lead to different levels of this substance being released in the brain,” Dr. Henrik Walter,

Director of the Research Area Mind and Brain at the Psychiatric University Clinic at the Charite in Berlin, said.

A total of 33 healthy probands were divided into two groups: One with the genetically stronger dynorphin release and the other which exhibits less gene activity.

Equipped with computer glasses the probands observed blue and green squares which appeared and then disappeared again in a magnetic resonance tomograph (MRT).

When the green square was visible the scientists repeatedly gave probands an unpleasant stimulus on the hand using a laser. Scientists were able to prove that these negative stimuli

actually led to a stress reaction given the increased sweat on the skin.

At the same time, researchers recorded the activities of various brain areas with the tomograph. After this conditioning stage came part two of the experiment: The researchers showed the

colored squares without any unpleasant stimuli and recorded how long the stress reaction acquired earlier lasted.

 The next day the experiment was continued without the laser stimulus in an effort to monitor the longer-term development.

It became apparent that, as in mice human, probands with lower gene activity for dynorphin exhibited stress reactions lasting considerably longer than those probands who released

considerably more.

Moreover, in brain scans it could be observed that the amygdala – a brain structure in the temporal lobes that processes emotional contents - was also active even if in later testing rounds a

green square was shown without the subsequent laser stimulus.

“After the negative laser stimulus stopped this amygdala activity gradually became weaker. This means that the acquired anxiety reaction to the stimulus was forgotten,” Walter said.

This effect was not as pronounced in the group with less dynorphin activity and prolonged anxiety.

“But the ‘forgetting’ of acquired anxiety reactions isn’t a fading, but, rather, an active process which involves the ventromedial prefrontal cortex,” Walter said.

To corroborate this, researchers found that in the group with less dynorphin activity there was reduced coupling between the prefrontal cortex and the amygdala.

“In all likelihood dynorphins affect fear forgetting in a crucial way through this structure,” Walter added.