Most of us experience anxiety at one point or another in our lives. While there are many different drugs and therapies currently available on the market, many of them come with a range of unwanted side effects. However, Weill Cornell Medicine researchers state that they have made significant advances in reducing anxiety by targeting specific areas of the brain. This means that we could soon have treatments available for anxiety that are more effective than current therapies and aren’t accompanied by any of the usual side effects.
The Study On Metabotropic Glutamate Receptor 2
The researchers from Weill Cornell Medicine recently published a study in the Neuron journal. Their goal was to explore how metabotropic glutamate receptor 2 (mGluR2), a brain receptor, could potentially be targeted to manage symptoms related to anxiety. The issue is that these receptors are spread all across the brain, making it difficult to develop drugs that can effectively activate them without resulting in unwanted cognitive side effects. However, this new study suggests that activating these receptors with a specific circuit that is connected to the amygdala may potentially provide relief without any of the usual side effects. The amygdala is a part of the brain that is linked to emotional regulation.
Read More: Six Natural Ways To Help You Get a Better Sleep
A Cure For Anxiety?
The research was led by an associate professor of biochemistry, Joshua Levitz. The study included extensive experimentation with pharmacological compounds meant to activate mGluR2 in the brain. The study revealed that, whereas these receptors are found in many brain circuits, targeting their function in a single circuit can ultimately result in better therapeutic effects. The scientists discovered that the basolateral amygdala was the part most responsible for the anxiety-reducing effects.
Isolating Pathways
Using genetic methods and specially developed tracer viruses, the researchers managed to identify two separate neuronal routes that led to the basolateral amygdala. In mice models, each pathway connected mGluR2 stimulation to anxiety symptoms. Using a method developed by Levitz, photopharmacology, the team used light-sensitive molecules to activate mGluR2. Illuminating these molecules with precise light wavelengths has the potential to influence receptor function in specific brain regions. The experiments produced inconsistent results. Activating mGluR2 in one circuit of the ventromedial prefrontal cortex reduced spatial avoidance, a common anxiety characteristic. However, this advantage was outweighed by a reported reduction in working memory, indicating the cognitive issues typically associated with traditional anxiety therapies.
Activating From the Insula
The results were more encouraging when mGluR2 was activated in the second circuit linking to the basolateral amygdala from the insula. This is a region of the brain that assists in integrating sensory information with internal body signals. This intervention improved social behavior and normalized patterns without impairing the person’s memory. These findings indicate that the insula-BLA circuit could be a suitable target for prospective anxiety treatments without the undesired cognitive side effects. According to the researchers, future studies should focus on developing medicines that specifically target the insula-BLA pathway rather than depending on mGluR2, which is widespread throughout the brain.
The Bottom Line
While the research is still in its infancy, it lays the groundwork for developing therapies that could help alleviate anxiety-related issues while presenting fewer side effects. The research group intends to continue developing methods and exploring different drug categories, such as antidepressants and opioids, using the same circuit-mapping technique. Who knows what other discoveries lay hidden deep within our own brain circuitry, potentially unlocking the door for anxiety treatment as well as other similar conditions?
Read More: Woman Diagnosed with ADHD Later in Life Reveals Three Key Traits Often Overlooked