Researchers fix amygdala circuit, reverse anxiety
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- Juan Lerma led the study at the Synaptic Physiology laboratory of the Institute for Neurosciences (IN), a joint CSIC and Miguel Hernández University center, and the results were published in iScience.
- Álvaro García reported that normalizing Grik4 gene activity in the basolateral amygdala restored communication with regular‑firing inhibitory neurons in the centrolateral amygdala, reversing anxiety‑related and social deficit behaviors in mice.
- Grik4 gene overexpression increased GluK4 glutamate receptors, making certain amygdala neurons hyper‑excitable and producing anxiety‑like and social withdrawal behaviors in the engineered mouse model.
- Basolateral amygdala neurons were targeted with viral‑mediated genetic tools to correct the imbalance, leading to dramatic improvements in standard anxiety and social interaction tests.
- Wild‑type mice with naturally elevated anxiety also showed reduced anxiety after the same circuit‑normalizing intervention, indicating the mechanism is not limited to the specific genetic model.
- Object recognition memory deficits persisted after treatment, suggesting other brain regions such as the hippocampus may contribute to aspects of the disorder.
- Spanish State Research Agency and other regional funders (Severo Ochoa Excellence Program, European Regional Development Fund, Generalitat Valenciana) funded the research.
Why it matters: The discovery gives neuroscientists and drug developers a concrete neural target for anxiety and related affective disorders, showing that correcting activity in a specific amygdala circuit reverses symptoms in both genetically engineered and normal mice, which could enable more precise, potentially more effective treatments with fewer side effects.
