By finding a level of nicotine at which cigarettes lose their addictive hook, the research has gotten closer to "breaking the relationship between nicotine and this deadly product".
We used a licenced nicotine patch, a warranty of validated bioavailabilty, which allowed the findings of the nicotine patches to be generalised to clinical practice.
Our findings regarding expression of TH protein in the VTA indicate a fine agreement with previous findings that injection of nicotine elevates the extracellular DA levels and its metabolites in the VTA [ 20, 38].
These data regarding the striatum are consistent with previous findings in rodents of nicotine sensitization of dopamine release especially in nucleus accumbens following repeated administration.
Nonetheless we did not find a benefit of nicotine consumption in terms of life expectancy of infected bees, making these findings difficult to interpret.
Consequently, there has been continuing controversy in the literature about the validity of previous findings of reinforcing effects of nicotine in experimental animals and human subjects [3], [4], [5], [6], [7], [8].
However, should the findings be in favour of nicotine e-cigarettes without additional adverse effects then it will establish a new balance between clinical benefit and harm for three month's use of e-cigarettes.
The induction of c-Fos protein in the NAc and striatum indicated a fine agreement with the previous findings that repeated injection of nicotine elevates the extracellular DA levels and its metabolites in the NAc and striatum [ 20].
The current finding that a single injection of nicotine can cause rectification has also recently been confirmed by another group [33].
This is in agreement with the finding elsewhere that 24 hours of nicotine incubation of human coronary artery endothelial cells had no effect on the expression of ET-1 [ 35].
