Roughly a third of all Americans experience an anxiety disorder at some point in their lives. These ailments include general anxiety disorder, severe phobias, panic disorder, social anxiety disorder, and post-traumatic stress disorder. They’re often treated with mental health therapy or medications.

For instance, benzodiazepines are a class of anti-anxiety drugs that are generally effective and well-tolerated; however, they come with problematic drawbacks. They can be addictive, interact dangerously with certain other drugs, and often trigger wide-ranging side effects such as drowsiness, confusion, headache, nausea, and tremors.

These drugs work by enhancing the activity of receptors that respond to an inhibitory neurotransmitter called gamma-aminobutyric acid (GABA). GABA reduces the excitability of neurons throughout the nervous system, essentially slowing down most bodily processes. This global deceleration also triggers the benzodiazepines’ calming effect. Familiar brand names of the drug include Valium, Xanax, Ativan, and Klonopin.

The NINDS team wondered if there was a better, more precise way to treat anxiety — one that wouldn’t trigger body-wide side effects. So, they stressed out mice until the animals developed clear signs of chronic anxiety when compared to their healthy, unstressed companions. For example, they were less willing to explore new areas, engaged in more repetitive behaviors, and avoided social interactions.

It was almost as if the researchers found an off-switch for anxiety in the mouse brain.

The researchers then searched for differences between the brains of anxious and unstressed mice. They noticed that levels of two neurotransmitter proteins, Neuroligin2 and GABA, were markedly decreased in the anxious mice. Already aware of GABA’s ability to lessen anxiety, they focused on Neuroligin2. With further probing, the researchers determined that chronic stress enhances the activity of a protein called Src kinase, triggering a cascade of effects called a signaling pathway that results in less circulating Neuroligin2. They wondered, Would suppressing Src kinase’s activity help alleviate the rodents’ anxiety?

To find out, Pandey, Lu, and their colleagues injected the anxious mice with an Src-inhibiting therapeutic called PP2 once daily for seven days. The effects were astounding. With less Src activity, its corresponding signaling pathway slowed to a standstill, resulting in higher Neuroligin2. Outwardly, the animals’ anxious behaviors disappeared. Moreover, there were no noticeable adverse effects. It was almost as if the researchers found an off-switch for anxiety in the mouse brain….’ (Big Think)