Sentence examples for sensitivity to nicotine from inspiring English sources

Additionally, two mutations (S516D and T536A) that displayed normal activation with ACh displayed remarkable reductions in sensitivity to nicotine.

Conclusions: The data suggest that increased sensitivity to nicotine as manifested by relaxation, dizziness, or nausea in response to the first exposure to nicotine represents a risk factor for the development of nicotine dependence.

People's sensitivity to nicotine varies.

Initial sensitivity to nicotine constitutes an early predictor of the vulnerability to developing nicotine dependence among novice smokers [ 72– 72].

Support for this hypothesis has come from evidence suggesting that genetic polymorphisms related to D4 and D2 receptors appear to modulate initial sensitivity to nicotine [ 14].

To date, a total of 10α and 4β different subunits have been described on the basis of the receptors sensitivity to nicotine [ 11].

A potential explanation for this finding is that the experience of unpleasant sensations reflects an increased sensitivity to nicotine-induced dysphoric effects (e.g. nausea) [ 5] that is not as amenable to the effects of tolerance as those with decreased sensitivity to nausea [ 29].

The transmembrane receptors for ACh (AChR) are classified according to their relative sensitivities to nicotine and muscarine.

Even though craving is generally the first symptom of dependence, even earlier phenotypes of the risk of nicotine dependence can be distinguished, such as sensitivity to the first dose of nicotine (i.e., experience of rewarding or aversive sensations).

One animal experiment found that 5-time nicotine administrations at 3-day intervals developed a significant locomotor stimulant effect and caused an enhanced sensitivity (cross-sensitization) to MA, although nicotine had no effect at first administration [ 49].

To this end, we used a BAC transgenic mouse model overexpressing the human CHRNA5/A3/B4 gene cluster (Tg CHRNA5/A3/B4), which exhibit increased sensitivity to the pharmacological effects of nicotine [ 37], along with increased binding sites for nicotinic agonists in hippocampal membrane preparations [ 38] and hippocampal slices, particularly in the CA1 region [ 37].