Neuroscientists Find Brain Circuit That Drives Anxiety

Mental Health News: Neuroscientists have identified a neural circuit in the amygdala that gives rise to anxiety. They found the critical role of a molecule called dynorphin, which could serve as a target for treatment of anxiety-related disorders.

Anxiety is the most common brain disorder affecting about 18% of the adult US population. Previous studies indicate that two regions in the amygdala — the central amygdala and the BNST — coordinate short-term and long-term responses to various kinds of threatening stimuli.

Neuroscientists at Cold Spring Harbor Laboratory aimed to find the underlying circuit and cellular mechanisms in these regions that control the generation of anxiety. The research team genetically manipulated one specific type of neuron called SOM+ because of a peptide they express called somatostatin.”SOM+” neurons are necessary for the learning of fear responses.The team knocked out a gene linked to bipolar disorder and schizophrenia called Erbb4 in SOM+ neurons in the central amygdala.

The experiment results showed heightened anxiety in mice. The team traced the mechanism behind this anxiety within a circuit that runs between the central amygdala and the BNST. They found that deleting Erbb4 increased excitation of SOM+ neurons, which led to a large increase in signaling by dynorphin, a peptide made by these neurons. This process disturbed the normal in inhibition of SOM+ neurons in the BNST, making them overactive.

Research concludes that Dynorphin signaling drives anxious behavior in people. By manipulating this circuit in mice, the team was able to lower anxiety. Therefore, Dynorphin could be a cellular target for Neuroscientists for future anti-anxiety drugs.

To Know More, You May Refer To:

Ahrens, S., Wu, M. V., Furlan, A., Hwang, G., Paik, R., Li, H., Penzo, M. A., Tollkuhn, J., & Li, B. (2018). A central extended amygdala circuit that modulates anxiety. The Journal of Neuroscience, 38(24), 5567-5583. https://doi.org/10.1523/jneurosci.0705-18.2018