Scientists reverse anxiety by fixing a tiny brain circuit
9 reported
Researchers at the Institute for Neurosciences, a joint center of the Spanish National Research Council and Miguel Hernández University of Elche, have identified a specific brain circuit in the amygdala that appears to play a major role in anxiety, depression-like behaviors, and social withdrawal. In a study published in iScience, the team led by Juan Lerma found that restoring balance within this circuit reversed several of these behaviors in mice. The research focused on a group of neurons in the basolateral amygdala, where normalizing activity of the Grik4 gene restored communication with inhibitory neurons in the centrolateral amygdala. The intervention reversed anxiety-related and social deficit behaviors in genetically engineered mice that displayed unusually high levels of the Grik4 gene. The same treatment also reduced anxiety in wild-type mice that naturally showed elevated anxiety levels. However, the mice continued to show deficits in object recognition memory after the intervention, suggesting other brain regions may be involved.
What’s reported
The study was led by Juan Lerma and his team at the Synaptic Physiology laboratory at the Institute for Neurosciences, a joint center of the Spanish National Research Council and Miguel Hernández University of Elche.
The findings were published in iScience.
Researchers used genetically engineered mice that produced unusually high levels of the Grik4 gene, increasing the number of GluK4 glutamate receptors and making certain neurons more excitable.
The mouse model was originally developed by the same laboratory in 2015.
By normalizing Grik4 gene activity in the basolateral amygdala, researchers restored communication with regular firing neurons in the centrolateral amygdala.
The intervention reversed anxiety-related and social deficit behaviors in the genetically engineered mice.
The same intervention reduced anxiety in wild-type mice that naturally displayed elevated anxiety levels.
The mice continued to show deficits in object recognition memory after the intervention.
The study was supported by funding from the Spanish State Research Agency, the Severo Ochoa Excellence Program, the European Regional Development Fund, and the Generalitat Valenciana.
Key figures
Juan Lerma, researcher at the Synaptic Physiology laboratory at the Institute for Neurosciences (joint center of CSIC and UMH)
Álvaro García, first author of the study
M. Isabel Aller, co-author
Ana V. Paternain, co-author
Sources: ScienceDaily
