The synthetic analogue of psychedelic will allow to treat depression and addiction without causing hallucinations

An artificial analog of ibogaine has been obtained, which stimulates the restoration of connections between neurons without side “psychedelic” and toxic effects.

Ketamine, LSD, and other “psychoactive” substances are considered as potential treatments for alcoholism and other addictions, as well as depression. Indeed, these states are accompanied by a loss of connections between neurons in the prefrontal cortex, responsible for decision making and other higher cognitive functions. And already relatively small doses of “psychedelics” stimulate the formation of dendritic spines on neurons – outgrowths that strengthen the connections between them. Meanwhile, doctors are stopped by the “psychoactive” and often toxic effects of these substances on the body.

Therefore, many scientists are busy looking for analogs of these compounds that would also positively affect neurons but would not have unnecessary and dangerous side effects. The team of David Olson of the University of California, Davis, took ibogaine, the active ingredient in a plant called iboga, used by sorcerers of Bwiti’s African cult, as the basis for this work. They write about the results of this work in an article published in the journal Nature.

In addition to its “psychedelic” effect, ibogaine causes heart rhythm disturbances and other dangerous symptoms. In their search for less toxic analogs, Olson and colleagues synthesized 20 closely related chemical compounds that retain the molecule region believed to be responsible for the “beneficial” properties, but without side groups associated with side effects. Having tested new substances, scientists have chosen the most promising – tabernanthalog (tabernanthalog, TBG).

Experiments on cell cultures of neurons and living laboratory rodents, have confirmed that TBG stimulates the formation of dendritic spines without causing visible side effects. TBG also removed alcohol and heroin cravings in model mice and rats addicted to these drugs. The authors note that the molecule did not lead to the activation of the “pleasure centers”, which means that it should not potentially cause addiction.

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