Oral ketamine is a popular treatment for severe depression. It can be used as both an anesthetic or recreational drug.A single dose of the psychedelic drug has been proven to stop suicidal thoughts within hours. Recent clinical trials have shown that these effects last for several weeks and are effective on up to two thirds of patients.Oral ketamine nasal spray is now available in the United States to treat chronic depression and suicidal thoughts.We still don't know how much the drug has antidepressant properties, despite its increasing use in the United States. There are many receptors that Ketamine can interact with in the brain. But which ones lead to antidepressant effects?Scientists believe that ketamine's therapeutic properties are due to its ability to influence glutamate, which is a neurotransmitter secreted at the brain's ends. While ketamine may increase glutamate production in certain brain areas in mice and humans, it seems to decrease its release in other brain regions."Elevated glutamate production has been linked with stress, depression, and other mood disorders," says Per Svenningsson, a neuroscientist from Sweden's Karolinska Institutet.New results from experiments on mice and their neurons support this hypothesis, at least for the prefrontal cortex. This is linked to complex cognitive behavior, emotion modulation, and complex cognitive behavior.Svenningsson, along with colleagues, measured glutamate levels in free-moving and anesthetized mice and found that ketamine reduced the persistent release of this neurotransmitter almost instantly.Researchers noticed an immediate reduction in extracellular glutamate levels after injecting ketamine into a mouse's prefrontal cortex. This was within just 30 minutes. The authors also observed similar results in normal mice as well as mice with depression-like symptoms.The authors state that these effects could be a contributing factor to the effectiveness of ketamine in instantly relieving depressive symptoms and suicidal thoughts.Further examination under the microscope shows that ketamine acts upon the neurons that receive glutamate. This causes these cells to release more of the neurotransmitter adenosine.The synapse is where adenosine enters the space between the neurons. It tells presynaptic cells to stop producing glutamate.To test the role of ketamine receptors in the postsynaptic neurons, researchers were able to block them and stop the loss of glutamate from their presynaptic neurons.Svenningsson says, "This suggests that the antidepressant effect of ketamine could be regulated through a feedback mechanism.""It's new knowledge that can help explain some of the fast effects of ketamine."Ketamine's fast inhibitory effect could explain why it is so effective in treating depression symptoms. Recent research has shown that stress-induced depression in mice models and anxiety-like behavior in mice models was caused by certain cells in the cerebrospinal Fluid.Oral ketamine is a side effect of antidepressants that can be used to treat severe depression.Ketamine, a psychoactive drug, can cause fatigue, anxiety, restlessness, dizziness, dizziness, and hallucinations. It is difficult to treat clinically.Scientists are now trying to determine if they can quickly treat depression with ketamine without including the unwanted side effects.Maybe it's the hallucinogenic components that make the medicine work. We don't know enough to be certain, so we need to find out more about ketamine and its powerful antidepressant properties.Drug engineers might be able to mimic the antidepressant effects most prominently displayed by glutamate. They could create a safer alternative with far fewer side-effects, but that still works as fast and aggressively as ketamine.Scientists have so far only created two non-hallucinogenic drugs similar to ketamine. These drugs are not specifically designed to target glutamate production and have been only tested on mice. However, the drugs showed rapid anti-depressant effects and did not cause the typical head twitches that can be caused by ketamine.Although the research so far is based on animal models only, if the results prove promising enough clinical trials could be in the future for humans.The study was published by Molecular Psychiatry.