Letting the brain take the strain

Neuroscientists at the University of Leicester, in collaboration with researchers from Poland and Japan, announced the discovery of a critical and previously unknown pathway in the brain that is linked to our response to stress.
Letting the brain take the strain
An illustration of the structures of the limbic system of the brain, the complex network of nerve pathways involved with expression of human instinct and mood. Regions are colourcoded as follows: the reticular formation (purple); the thalamus (pink); the hypothalamus (orange); green body overlying top of hypothalamus is the mamillary body; yellow body below the hypothalamus is the amygdala; yellow body beneath the amygdala is the hippocampus; large yellow body<br /> at top, left of the thalamus, is the caudate nucleus. Activities governed by the limbic system include self-preservation, reproduction, expression of fear, rage, pleasure, and the formation of memory. John Bavosi/Science Photo Library

An international team of researchers led by Leicester announced a breakthrough in identifying a chain of chemical processes in the brain that trigger our response to highly stressful and traumatic events.

Why is it that some of us can experience highly stressful events and ‘soldier on’ while others suffer depression, anxiety or post-traumatic stress disorder?

The reasons for this are not clear, prompting an international investigation that has led to a new discovery announced in the prestigious scientific journal, Nature.

Neuroscientists at the University of Leicester in collaboration with researchers from Poland and Japan, announced the discovery of a critical and previously unknown pathway in the brain that is linked to our response to stress. The advance offers new hope for targeted treatment, or even prevention, of stress-related psychiatric disorders.

Dr Robert Pawlak, from the University of Leicester who led the UK team, said: “Stress-related disorders affect a large percentage of the population and generate an enormous personal, social and economic impact. It was previously known that certain individuals are more susceptible to detrimental effects of stress than others. Although the majority of us experience traumatic events, only some develop stress-associated psychiatric disorders such as depression, anxiety or post-traumatic stress disorder. The reasons for this were not clear.”

Dr Pawlak added that a lack of correspondence between the commonness of exposure to psychological trauma and the development of pathological anxiety prompted the researchers to look for factors that may make some individuals more vulnerable to stress than others.

The study found that the emotional centre of the brain – the amygdala – reacts to stress by increasing production of a protein called neuropsin. This triggers a series of chemical events which in turn cause the amygdala to increase its activity. As a consequence, a gene is turned on that determines the stress response at a cellular level.

“We then examined behavioural consequences of the above series of cellular events caused by stress in the amygdala,” said Dr Pawlak. “Studies in mice revealed that upon feeling stressed, they stayed away from zones in a maze where they felt unsafe. These were open and illuminated spaces they avoid when they are anxious.

“However when the proteins produced by the amygdala were blocked – either pharmacologically or by gene therapy – the mice did not exhibit the same traits. The behavioural consequences of stress were no longer present. We conclude that the activity of neuropsin – previously discovered by Professor Sadao Shiosaka, a co-author of the paper – and its partners may determine vulnerability to stress.”

The study took four years to complete, during which scientists from the Department of Cell Physiology and Pharmacology collaborated with colleagues from the Medical Research Council Toxicology Unit at the University of Leicester, the Department of Molecular Neuropharmacology, Polish Academy of Sciences in Krakow, Poland and Nara Institute of Science and Technology in Japan. The work was supported by the European Union, the Medical Research Council and Medisearch – the Leicestershire Medical Research Foundation.

This article originally appeared in LE1 Autumn 2011.

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