Ketamine is an anaesthetic and analgesic substance. It is mainly used to make you insensitive to pain and to relieve from pain. Although it has been related to side effects as a result of abuse, the World Health Organization concluded that it was not a threat for becoming a global public health issue. But ketamine doesn’t only relieve pain but it also treats depression and this is the topic of this article.

The study to which we’ll refer to is “NMDAR-independent, cAMP-dependent antidepressant actions of ketamine.”. It is published in Nature’s Journal of Molecular Psychology and conducted by researchers at the University of Illinois at Chicago. It is a fact that scientists knew about the anti-depression properties of ketamine but the mechanism wasn’t clear. Depression happens as a result of an increased number of G proteins. G proteins are responsible for producing the cyclic AMP (cAMP) which is a messenger taking part in substantial biological processes. This “messenger” appears to be discouraged by G proteins which are numerous in cell membranes. These G proteins don’t have the main function of stopping the cAMP. Instead, they do it because they are numerously stuck in cell membranes.

Ketamine appears to free those membrane-stalled G proteins and make them work properly again. Ketamine does this faster than the most known antidepressants. Have a look at what Mark Rasenick, a professor at the UIC College of Medicine, told for the online UIC today:

When G proteins move out of the lipid rafts, it allows for better communication among brain cells, which is known to help alleviate some of the symptoms of depression.Whether they are moved out by traditional antidepressants or ketamine, it doesn’t matter, although with ketamine, the G proteins are very slow to move back into the lipid rafts, which would explain the drugs long-term effects on depressive symptoms.

The professor continues by saying that the movement of G proteins from the lipid rafts is a biomarker of the effectiveness of a given antidepressant. He concludes that:

It confirms that our cell model is a useful tool for showing the effect of potential new antidepressant drug candidates on the movement of G proteins and the possible efficacy of these drugs in treating depression.