Theoretically has been that the vitamin works by preventing brain receptors called GLUN1-2B-2D. Here, we see one of the many ways that the chemical particles of the drug (yellow) can be associated with a specific part (gray network) of brain receptors. Credit: Furukawa Lab/CSHL
The ketamine received a transformation of Hollywood. It was known as delirium drugs (private street name K) and cat anesthesia. However, in recent years, some of the vitamin doctors to treat cases of post -traumatic disorder to depression. “This practice is not without controversy,” notes a professor of CSHL Hiro Furukawa.
“Should we give the patients to patients in mental cases?” The skeptical ketamine. The controversy came to his head in 2024 after the death of Matthew Perry. The famous television actor died of an overdose of ketamine. One person assigned to the death of Perry was the doctor who was prescribed by the vitamin for depression and anxiety.
“Until this is aside, many questions remain in terms of how the vitamin affects the brain.” “It has been suggested for more than a decade that the drug prevents a certain type of NMDA (NMDAR) receptors, called Glun1-2B-2D.”
There was a big problem with this theory. Scientists were not completely sure of the presence of Glun1-2B-2D. A new study from the Furukawa Laboratory lights the light that is needed on the situation.
In a paper published in the magazine Nerve cellsFurukawa and postdoc hyunook kang prove that Glun1-2B-2D is in the mammal brain.
Then rebuild a human version of Glun1-2B-2D. Do not stop there. Using a CRYO-AEm, they pick up Glun1-2B-2D while working.
Neuroscientists define the mechanism of tension and release that controls Glun1-2B-2D movements. They can now see how this mysterious NMDAR opens and closes the ion channel pores. And they go another step forward. They reveal several methods that may be associated with Glun1-2B-2D.
A series of staggering detailed perceptions shows that ketamine molecules have become connected to specific parts of the Glun1-2B-2D. “It is like a network,” explains Forocawa.
“On small fractures of a second, the mites can hold these sections and close the channel.” Furukawa and his colleagues captured four binding patterns. However, they believe that there are many other methods that can be controlled by ketamine.
It is believed that ketamine may relieve the symptoms of depression and anxiety by affecting the Glun1-2B-2D movement. But how long should the channel remain open or closed?
“This is more likely to differ for every patient,” says Furokawa. Likewise, the side effects of the treatment of ketamine can range from light hallucinations to complete psychosis. However, if scientists can determine how Glun1-2B-2D movements affect the brain, they may be able to manufacture new versions of the drug with less harmful side effects.
It can provide hope for millions of people with depression and anxiety. Therefore, this is where Furukawa and his colleagues in CSHL will be their eye after that.
More information:
The structural basis of the channels of the channel and the blockade in the NMDA TIDA-HETEROMERICEC GLUN11-2D receptors, Nerve cells (2025). DOI: 10.1016/J.neuron.2025.01.013. www.cell.com/neuron/fulltext/S0896-6273(25)00039-X
Introduction from the Cold Spring Harbor Laboratory
quoteCitamine research may lead to safer treatments for depression, anxiety and other mental health conditions (2025, February 14) that were recovered on February 14, 2025 of https://medicalxpress.com/news/2025-02-Ketamine-safer. Anxiety
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