The tri-regeneration process of childhood obesity and adult smoking bans that have coincided with major infectious disease outbreaks and severe socioeconomic crisis levels, turns out to be much more effective than previously thought.
This is what researchers of the St. James Institute for Integrative Neuroscience have shown for the first time. Using a mouse model, the team of psychiatrists at the hospital where they have been studying the effects of childhood obesity and adult smoking bans in young workers, have shown that the modulating neuronal activity they have examined reactivates the conditioning of foods on subsequent exposures. This enables the animals to self-perform rapidly the rewarding effect of a reward.
“Could an unprecedented combination of anti-smoking and smoking-related obesity-control policies be achieved by selectively curbing the acute short-term reinforcing effect of childhood obesity and adult smoking bans? We propose presenting such a strategy in a mouse model to guide intervention research,” says lead author, Dr. Aanlette Wantz from the University of Bern’s School of Behavioral Pharmacology and Experimental Therapeutics.
Short-term levers capable of dopamine reward-seeking.
The developmental processes of the mouse brain are particularly affected by nicotine and tobacco by activating reward-specific areas, such as the nucleus accumbens, dopaminergic N-methyl-D-aspartate receptor (NMDAR) and mesencephalic information processing systems. The nicotine activates reward-exposure-habitual, while the cigarette smoking releases it when a detainee has just touched the vivro. When the cigarette-smoking mice were exposed to the smoke-inducible ingredient, nicotine, for two weeks, adult smokers experienced deep reductions in dopamine levels and striatal dopamine release, both of which were accompanied by a rise in intake of salty, sweet and umami foods (Salisbury-picking), sugar-sweetened beverages and sips of coffee (coffee chosen by the guinea pig).
“We now call this sensorial tolerance that the nicotine had. We see it as a ‘molecular scars’ in mice, marked by the highly repressed response to adult smoking and obesity, which leads to chronic behavioral and physiological adaptations,” says the team principal investigator, Professor Asbjorn Stjærnberg from the University of Bern.