Where anxiety is located
Scientists find out which cell type within the anxiety brain circuits is crucial for behavorial symptoms
Stress can increase anxiety. The stress hormone cortisol acts on glucocorticoid receptors to mediate anxiety. How are different cell types that express this receptor involved? Scientists at the Max Planck Institute of Psychiatry were able to prove for the first time that it is not only the brain region but also the different types of neuronal populations that play a pivotal role. This finding may provide a new approach for the treatment of anxiety disorders.
Around 20 percent of the population suffer from an anxiety disorder at some point in their lives. Very often, anxiety is concomitant with other psychiatric disorders. For example, 60 to 70 percent of people suffering from depression are also troubled by anxiety.
Scientists know in which brain regions anxiety is generated, e.g., in the amygdala, and that stress can increase anxiety. This knowledge is important since many of the underlying diseases associated with anxiety are also stress-related.
What the scientists did not know previously, is whether a certain type of brain cell is responsible. The main receptor for the stress hormone cortisol, the glucocorticoid receptor, mediates anxiety. Which type of neurons, however, mediates this effect? When neurons make the messenger glutamate they act excitatory, whereas if they secrete GABA, they inhibit neuronal activity. This is the issue scientists working with Mathias Schmidt at the Max Planck Institute of Psychiatry have been investigating.
In a mouse model, Schmidt and his team blocked the glucocorticoid receptor expression only in either the excitatory glutamatergoc neurons or the inhibitory GABAergic neurons. Their results, now published in the renowned journal ‘Molecular Psychiatry’, show: Only mice lacking glucocorticoid receptors in glutamatergic neurons were less anxious. The other group, in which the GABAergic neurons’ receptors had been deleted, did not show any differences in anxiety. Thus, the cell population seems to be decisive in the development of stress-induced anxiety.
In a second step, the researchers studied a smaller area within the brain, i.e., only the amygdala. Here, the results were even more specific, showing that the glucocorticoid receptor plays a role in modulating fear memory.
Of particular interest for the scientists at the Max Planck Institute was the fact that the effects of stress-induced anxiety and fear can be assigned to different brain regions. This finding provides valuable evidence supporting differentiated treatment of anxiety and fear.
Even more important is the newly gained understanding that, in addition to the brain region, the cell type is decisive. This is relevant for the treatment of anxiety disorders because it provides an indication as to precisely which circuits are responsible for anxiety and where to target drug therapy.