孕烯醇酮可保护大脑免于大麻影响

Two INSERM research teams led by Pier ¹ Vincenzo Piazza ² and Giovanni Marsicano (INSERM Unit 862 "Neurocentre Magendie" in Bordeaux) recently discovered that pregnenolone（孕烯醇酮）, a molecule ³ produced by the brain, acts as a natural defence mechanism ⁴ against the harmful effects of cannabis in animals. Pregnenolone prevents THC, the main active principle in cannabis, from fully ⁵ activating ⁶ its brain receptor, the CB1 receptor, that when overstimulated by THC causes the intoxicating ⁷ effects of cannabis. By identifying this mechanism, the INSERM teams are already developing new approaches for the treatment of cannabis addiction ⁸. These results are to be published in Science on 3 January., ,Over 20 million people around the world are addicted ⁹ to cannabis, including a little more than a half million people in France. In the last few years, cannabis addiction has become one of the main reasons for seeking treatment in addiction clinics. Cannabis consumption is particularly high (30%) in individuals between 16 to 24 years old, a population that is especially susceptible ¹⁰ to the harmful effects of the drug., ,While cannabis consumers are seeking a state of relaxation ¹¹, well-being ¹² and altered perception, there are many dangers associated to a regular consumption of cannabis. Two major behavioural problems are associated with regular cannabis use in humans: cognitive ¹³ deficits ¹⁴ and a general loss of motivation. Thus, in addition to being extremely dependent on the drug, regular users of cannabis show signs of memory loss and a lack of motivation that make quite hard their social insertion., ,The main active ingredient in cannabis, THC, acts on the brain through CB1 cannabinoid receptors located in the neurons. THC binds ¹⁵ to these receptors diverting them from their physiological ¹⁶ roles, such as regulating food intake ¹⁷, metabolism ¹⁸, cognitive processes and pleasure. When THC overstimulates CB1 receptors, it triggers a reduction in memory abilities, motivation and gradually leads to dependence ¹⁹.