This study examined the role of Chrnb2 and Chrna5 on menthol consumption in mice. Data from our lab demonstrated that mice homozygous for the nicotine dependence risk allele for the human CHRNA5 SNP rs16969968 consumed more menthol by choice than mice homozygous for the reference allele.Ìý
(Drug and Alcohol Dependence, 2024)
In this study, we used Chrna5 knockout mice bred onto a panel of chromosome substitution strains to determine whether there might be genes that can alter the effect of Chrna5 on nicotine consumption. Results indicated that there are likely several genes that can eliminate the effect of Chrna5 deletion on nicotine consumption as well as genes that affect nicotine consumption independent of Chrna5. Because CHRNA5 is associated with nicotine dependence in humans, identification of these Chrna5 modifiers may lead to novel targets for the development of smoking cessation aids.
(Frontiers in Psychiatry, 2021)
We previously demonstrated that in utero nicotine exposure leads to neurodevelopmental disorder-like behaviors (ADHD, schizophrenia, autism, etc.) and altered brain biochemistry in both the directly in utero-exposed offspring and the unexposed grand-offspring. This study identified changes in several epigenetic factors which may explain the multi-generational effect of in utero nicotine exposure on behavior and brain biochemistry.
(Epigenetics & Chromatin, 2020)
This study was the first study to assess the effect of nicotine withdrawal in an animal model. Results indicated that nicotine withdrawal had little effect on overall sleep time but did lead to sleep fragmentation, a measure indicative of poor sleep quality. These findings are similar to the effect of nicotine withdrawal in humans.
(Psychopharmacology, 2019)
This paper describes a series of experiments that demonstrate that the effect of in utero and early post-natal nicotine exposure on adolescent nicotine consumption and striatal dopamine release are impacted by a genetic variant in the nicotinic acetylcholine receptor gene Chrna5. Following developmental nicotine exposure, mice possessing a "risk' variant for nicotine consumption increased nicotine consumption and exhibited reduced striatal dopamine release following developmental nicotine exposure while mice possessing the "non-risk" variant showed substantially reduced nicotine consumption and increased striatal dopamine release. These results suggest that nicotine consumption behavior and brain function are influenced by both genetics and environmental exposures.
