Researchers, at the Max Planck Institute for Experimental Medicine in Göttingen, have found a synaptic protein which on its inactivation has an anxiolytic effect in mice.
Anxiety disorders are a severe mental illness. It causes significant fear or worry that does not easily go away. It may even get worse over time. We all feel worried sometimes, but with an anxiety disorder, the anxiety tends to be fairly constant. And it has a negative and disturbing effect on a person’s quality of life.
In extreme cases, the affected persons hardly leave their homes. This can have serious consequences for their relations with family and friends as well as for their professional lives. About 10 percent of the population suffers from anxiety disorders. And current treatments only offer effective aid for a proportion of those affected.
Changes in amygdala
One of the changes observed in the brains of individuals with anxiety complaints is increased neuronal activity in the amygdala. This part of the brain is a region which is involved in processing emotions such as fear or anxiety. It’s over activation is thought to be involved in causing exaggerated anxiety.
Many anxiolytic drugs such as benzodiazepines apparently stabilize this overactivation by strengthening the function of inhibitory synapses. Actually, synapses are connections between nerve cells. These connections are involved in the transmission of information from one nerve cell to another.
At inhibitory synapses, this transmission results in a drop in the activity of the adjacent nerve cells. For instance, this inhibits the transmission of stimuli which generate fear and anxiety in the amygdala.
Benzodiazepines strengthen this inhibitory effect. But unfortunately, they affect not only those inhibitory synapses which conduct anxiogenic stimuli but also many other inhibitory synapses present in the brain.
This can cause significant side effects like pronounced sedation and weakened concentration. So, researchers are searching for more definite targets for anxiolytic medications.
Experiment on mice with anxiety disorder
Animal research with mice played a role to study anxiety disorders. While healthy animals curiously inspect an empty test chamber, rodents with an extreme anxiety phenotype withdraw into a corner as they are afraid.
Then, the researchers blocked the production of IgSF9b in these mice. After that, they began to move freely around the chamber again. IgSF9b is a recently discovered protein. It produces a protein bridge between two neighboring nerve cells at inhibitory synapses.
“Blocking IgSF9b protein in pathologically anxious animals has an anxiolytic effect. It normalizes their anxiety behavior. Therefore, this protein could be a target for pharmacological methodologies to treat anxiety disorders,” according to researchers.
An examination of the amygdala in mice revealed that the over-activation of the amygdala was normalized. This effect was due to the strengthening of the synaptic transmission at inhibitory synapses in the amygdala.
This research indicates that protein arrangements at inhibitory synapses in the centromedial amygdala, and mainly the protein IgSF9b, constitute encouraging new targets for probable treatments.
Thus, it provides a vital contribution toward understanding the biological causes of anxiety disorders. And for the development of new anxiolytic medications.