Acute Stress Causes Delayed Effects in the Brain

The molecular mechanism behind the delayed effects of acute stress has been identified.

Highlights.

Stress leads to the formation of new nerve connections in the amygdala called synapses.
These synapses lead to increased electrical activity in the amygdala, ten days after the stressful event.
The electrical activity is dependent on a molecule known as the N-Methyl-D-Aspartate Receptor (NMDA-R).

A single instance of severe and acute stress can lead to delayed and long-term psychological trauma.

The research team was led by Sumantra Chattarji from the National Centre for Biological Sciences (NCBS) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem), Bangalore.

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‘Blocking the protein, (N-Methyl-D-Aspartate Receptor), which is crucial for memory, helps to control the electrical activity that is triggered in the amygdala during the stressful period.’

The researchers explain the key molecular and physiological processes behind this mechanism.

Role of Amygdala

A stressful incident can trigger electrical activity in amygdala, not immediately, but after ten days.

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Amygdala is a small, almond shaped group of nerve cells in the temporal region of the brain. It plays an important role in emotional reactions, memory and decision making.

Post-Traumatic Stress Disorder or PTSD is an anxiety disorder that develops after a trauma or stressful event and its symptoms develop within three months after the experience. Changes in the amygdala are observed in PTSD.

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While experimenting with rats previously, Chattarji's group had shown that a single instance of acute stress had no immediate effects on the amygdala. But ten days later, these animals began to show increased anxiety, and changes in the amygdala.

"We showed that our study system is applicable to PTSD. This delayed effect after a single episode of stress was reminiscent of what happens in PTSD patients," says Chattarji. "We know that the amygdala is hyperactive in PTSD patients. But no one knows as of now, what is going on in there," he adds.

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New Synapses

Stress seems to have caused the formation of new nerve connections called synapses in the amygdala.

These new nerve connections in the amygdala lead to heightened electrical activity in this region of the brain with the help of a molecule known as the N-Methyl-D-Aspartate Receptor (NMDA-R)- a protein on nerve cells known to be crucial for memory functions.

This protein is important for memory and learning.

Blocking NMDA-R

When researchers blocked the NMDA-R during the stressful period, they observed that it:

stopped the formation of new synapses
blocked the increase in electrical activity at these synapses

"So we have for the first time, a molecular mechanism that shows what is required for the culmination of events ten days after a single stress," says Chattarji. "In this study, we have blocked the NMDA Receptor during stress. But we would like to know if blocking the molecule after stress can also block the delayed effects of the stress. And if so, how long after the stress can we block the receptor to define a window for therapy," he adds.

The study is published in the online only open-access journal Physiological Reports

Reference

Sumantra Chattarji et al. The delayed strengthening of synaptic connectivity in the amygdala depends on NMDA receptor activation during acute stress. Physiological Reports; (2016) DOI: 10.14814/phy2.13002

Source-Medindia