Anxiety disorders are the world’s most common type of mental health condition, impacting the lives of around 360 million people. But what if there was a way to reverse anxiety’s effects?
By ‘rebalancing’ just a few neurons in the amygdala – a part of the brain responsible for decision-making, recall, and managing emotions — researchers from the Spanish National Research Council and the Miguel Hernández University of Elche (CSIC-UMH) in Spain removed anxiety, depression, and social deficits in mice, returning their typical behaviors.
This rebalancing was done via a gene called GRIK4, which has an important role in brain messaging.
When overexpressed, GRIK4 increases the production of a protein called Gluk4, which triggers anxiety-like behaviors. Mice with more of the GluK4 protein tend to avoid open spaces, aren’t as comfortable socializing, and show signs of depression, for example. They also have trouble recognizing objects.
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Using gene editing techniques to cut out extra copies of the GRIK4 gene, the researchers reduced GluK4 in mice, eliminating signs of anxiety, depression, and social issues.
“That simple adjustment was enough to reverse anxiety-related and social deficit behaviors, which is remarkable,” says neuroscientist Álvaro García.
In addition, the team identified a specific type of neuron in the amygdala as responsible for the symptoms of anxiety. When these neurons were returned to a standard state, the mice’s behavior returned to normal.
The treated mice still struggled with object recognition memory tasks in subsequent tests, suggesting that other parts of the brain affected by anxiety disorders weren’t corrected by the dampened expression of GRIK4.
“We already knew the amygdala was involved in anxiety and fear, but now we’ve identified a specific population of neurons whose imbalanced activity alone is sufficient to trigger pathological behaviors,” says neuroscientist Juan Merma.
The same treatment was also successful when applied to non-engineered mice with higher anxiety levels, further demonstrating the crucial role localized parts of the brain have in anxiety disorders, and how these circuits could be rebalanced.
Though the same processes are yet to be observed in the human brain, mice are considered good scientific stand-ins, hinting at new treatments that could help calm our own overexcited, anxious brains. A technique similar to the one used in this study may be adapted for humans, providing relief from anxiety for many.
“Targeting these specific neural circuits could become an effective and more localized strategy to treat affective disorders,” says Lerma.
The research has been published in iScience.
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