This switch turns depression on and there may be a drug to turn it off

by time news

Glycine is an amino acid that also acts as a neurotransmitter, transmitting signals between neurons. Now, according to a study published in “Science”, it may become a target for drugs to treat depression. The study details that glycine signals in the brain and its antidepressant properties could be mediated by a receptor that the authors call mGlyR. The research describes this mechanism using computational models, in vitro assays, and experiments in mice.

This common amino acid, the wisteriayou can send a signal of «deceleration» to the brain, likely contributing to major depression, anxiety and other mood disorders in some people, scientists at the UF Scripps Wertheim Institute for Biomedical Innovation and Technology have found.

The discovery improves understanding of the biological causes of major depression and could accelerate efforts to develop new, faster-acting drugs for difficult-to-treat mood disorders.

“Most medications for people with depression take weeks before they take effect, if at all. Really new and better options are needed», says neuroscientist Kirill Martemyanov, author of the study.

The major depression It is among the world’s most urgent health needs. Their number has increased in recent years, especially among young people.

The researchers were trying to find out how sensors in brain cells receive and transmit signals. Therein lay the key to understanding vision, pain, memory, behavior, and possibly much more.

In 2018, Martemyanov’s team discovered that the new receptor was involved in stress-induced depression. If the mice lacked the receptor gene, called GPR158, they proved surprisingly resistant to chronic stress.

That offered strong evidence that GPR158 could be a therapeutic target.

In 2021, his team solved the structure of GPR158. What they saw surprised them. The GPR158 receptor looked like a microscopic clamp with a compartment, similar to something they had seen in bacteria, not human cells.

“We thought, that’s an amino acid receptor. There are only 20, so we looked at them right away, and only one fit the bill. It was wisteria,” says Martemy.

That wasn’t the only weird thing. The signaling molecule was not an activator in the cells, but an inhibitor. The commercial end of GPR158 attached to a partner molecule that hit the brakes instead of the accelerator when it bound to glycine.

“Usually, receptors like GPR158, known as G protein-coupled receptors, bind to G proteins. This receptor bound to an RGS protein, which is a protein that has the opposite effect of activation,” Thibaut says. Laboute first author of the study.

Scientists have been cataloging the role of cell receptors and their signaling partners for decades. Those that do not yet have known signalers, such as GPR158, have been termed “orphan receptors.”

The finding means that GPR158 is no longer an orphan receptor. Instead, the team renamed it mGlyR, short for “metabotropic glycine receptor.”

Labouté and Martemyanov are listed as inventors on a patent application describing methods for studying GPR158 activity. Martemyanov is co-founder of Blueshield Therapeutics, a start-up company pursuing GPR158 as a drug target.

Glycine itself is sold as a mood-enhancing nutritional supplement. It is a building block of proteins and affects many different cell types.

Glycine itself is sold as a mood-enhancing nutritional supplement. It is a building block of proteins and affects many different cell types, sometimes in complex ways. In some cells it sends slow down signals, while in other cell types it sends excitation signals. Some studies have linked glycine with the growth of prostate cancerthe invasive.

More research is needed to understand how the body maintains the correct balance of mGlyR receptors and how brain cell activity is affected, he said. He intends to continue like this.

«We need desperately new treatments for depression Martemyanov admitted. If we can address this with something specific, it makes sense that it could help.”

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