Washington : Scientists have identified a fat molecule in brain cells that may act as a ‘switch’ to increase or decrease the motivation to consume nicotine, a finding that could lead to new therapies to help smokers kick the butt, reports PTI.
“We knew these lipids were implicated in nicotine addiction, but until now manipulating their synthesis was not pharmacologically feasible,” said senior author Loren Parsons, professor at The Scripps Research Institute (TSRI) in US.
The motivation for natural rewards such as food, sex and exercise — and also of drugs such as nicotine — relies on neurons in the brain’s reward system, based in a brain region called the ventral tegmental area (VTA). Obtaining a reward leads to excitation of these neurons and the release of a neurotransmitter called dopamine, which acts on other neurons to trigger positive emotions.
The degree to which the reward system can be activated is normally tightly controlled. A neurotransmitter called GABA (gamma aminobutyric acid) inhibits excitatory signalling in neurons and keeps the system in balance.
Previous research indicated that chronic nicotine exposure boosts the excitation of dopamine signalling while decreasing the controls on this system by GABA’s inhibitory signalling. Nicotine exposure also leads to release of lipids called endocannabinoids, which affect dopamine-producing neurons.
Some researchers have tested potential anti-smoking therapies that block activity in the endocannabinoid receptor, where endocannabinoids bind. Although these treatments reduced the effects of nicotine on dopamine release and tended to reduce smoking, they also produced undesirable side effects, like depression and anxiety, that limited their clinical use, said Matthew Buczynski, Research Associate at TSRI.
The team hypothesised that instead of blocking endocannabinoid receptors throughout the brain, it would be more effective to specifically target the endocannabinoid mechanism that appears to be dysregulated by chronic nicotine.