Spanish scientists have identified neurons that regulate anxiety and for the first time demonstrated that adjusting a single gene can normalize their function.
Researchers from the Institute of Neuroscience in Spain have for the first time identified a specific population of neurons in the amygdala of the brain, whose excessive activity causes anxiety, depression, and social isolation. By correcting the expression of the gene Grik4, the scientists were able to restore the balance of neural networks in laboratory mice and completely eliminate pathological behavior.
Under the guidance of neurobiologist Juan Lerma, the team focused on the basolateral and central lateral areas of the amygdala. The former enhances emotional signals, while the latter — inhibitory neurons — normalizes stress responses. When this balance is disrupted, animals exhibited increased nervousness and avoided contact with their environment.
Genetic editing restored normal expression of Grik4 in the basolateral area, returning the neural networks to a balanced state. Mice that previously hid in dark corners began to freely explore their surroundings. A similar effect was confirmed in field mice with naturally high levels of anxiety.
The scientists note that some symptoms, such as difficulties in object recognition, persisted, indicating the involvement of other brain areas, including the hippocampus. Disruptions in glutamate signaling, controlled by Grik4, are also associated with autism, schizophrenia, and bipolar disorder.
If the mechanism is confirmed in humans, it will pave the way for targeted treatment methods for affective disorders that affect specific neural circuits rather than the entire brain.
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