The ability to experience fear is essential to escaping life-threatening situations and learning how to avoid them in the future. However, in some disorders, such as post-traumatic stress disorder and other anxiety-related disorders, the fear responses become excessive and persist even when they are no longer appropriate. This triggers a strong fear even though the danger is no longer there and means that the affected person cannot lead a normal life until the illness resolves. It has been suggested that certain individuals are more prone to pathological fears and that this is due to disorders in the brain’s processing of memories of frightening things.
Some areas of the brain are particularly important for processing fear-related memories. The amygdala is activated when threats are experienced and works in tandem with parts of the brain’s frontal lobe, called the “prefrontal cortex,” that are important in regulating emotions.
The network of nerve cells that connects the frontal lobes to the amygdala is known to be involved in anxiety management. The connections between these brain structures are altered in people with post-traumatic stress disorder and other anxiety disorders.
However, the molecular mechanisms involved were unknown for a long time.
In a new study, Estelle Barbier’s team at Linköping University in Sweden looked at a protein called PRDM2, an epigenetic enzyme that represses the expression of many genes. The researchers had previously found that PRDM2 levels are lower in alcohol dependent individuals, leading to exaggerated stress responses. Many people with alcohol addiction often also suffer from anxiety, and researchers have long suspected that this is because both problems are regulated by a common mechanism.
The research team, including Riccardo Barchiesi and Estelle Barbier, has discovered a biological mechanism that increases the strength with which frightening memories are stored in the brain. (Photo: Anna Nilsen / Linköping University)
For new memories to last, they must be stabilized and preserved as long-term memories. This process is called “consolidation”. The authors of the new study looked at the effects of reduced PRDM2 levels on the way memories of frightening events are processed in rats.
And they have confirmed that reducing PRDM2 increases consolidation of fear-related memories. Specifically, reduced levels of PRDM2 lead to increased activity in the frontal lobe-amygdala network, which in turn amplifies learned fear responses.
The researchers have also identified the genes that are affected when PRDM2 levels are reduced.
In short, the result of all this is increased activity in the nerve cells that connect the frontal lobes and the amygdala.
The study is titled “An epigenetic mechanism for overconsolidation of fear memories”. And it was published in the journal Molecular Psychiatry. (Font: NCYT by Amazings)