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Hunter Mathews

Research Associate

Institute for Behavioral Genetics

Institute for Behavioral Genetics
University of Colorado Boulder
447 UCB
Boulder, CO 80309-0447

Research Interests:

Investigating the effects of nicotine and abstinence on sleep behavior and diurnal rhythms. Identifying molecular and genetic mechanisms that mediate nicotine's effects on sleep, with a particular interest in the orexinergic system. Identification of genetic modifiers that contribute to nicotine dependence. The molecular characterization and validation of rare variants from phenotyping studies of nicotine dependence.

Mentors:

Jerry Stitzel

Active Grants:

5 U01 DA043802-04 (Stitzel), 04/01/18-12/31/22. Genetic modifiers of Chrna5 deletion in mice: role in nicotine behaviors modulated by the medial habenula-IPN pathway. Role Research Associate

5 R01 DA044283-03 (Vrieze), 05/01/19-02/29/24, Deep sequencing, phenotyping, and imputation in large scale biobanks: A novel and cost-effective framework to identify rare mutations associated with addiction. Role: Research Associate

Additional Resources:

Highlighted publications

Average (n = 9; ± SEM) active phase sleep latency across treatment periods. Baseline (BL), Abstinence Day (AD). *p < .05

The effects of oral nicotine administration and abstinence on sleep in male C57BL/6J mice

The present study was conducted to characterize sleep and wakefulness in male C57BL/6J mice during periods of oral nicotine administration and abstinence. Both oral nicotine administration and abstinence lead to sleep disturbances in mice. Similarities between this model and human reports on the effect of nicotine/nicotine withdrawal on sleep support its utility in examining the molecular mechanisms that modulate the relationship between sleep, nicotine, and nicotine abstinence/withdrawal.

(Psychopharmacology, 2019)

Schematic of the breeding strategy used to generate CSS possessing the Chrna5 null mutation. (A) Cross between a parental CSS and Chrna5KO mice on a B6 genetic background (B6Chrna5KO).

Genetic Modifiers of Oral Nicotine Consumption in Chrna5 Null Mutant Mice

The gene CHRNA5 is strongly associated with the level of nicotine consumption in humans and manipulation of the expression or function of Chrna5 similarly alters nicotine consumption in rodents. Toward a better understanding of how loss of function of Chrna5 increases nicotine consumption, we introgressed the Chrna5 knockout (KO) mutation onto a panel of C57BL/6J-Chr#A/J/NAJ chromosome substitution strains (CSS) and measured oral nicotine consumption in 18 CSS and C57BL/6 (B6) mice homozygous for the Chrna5 KO allele as well as their Chrna5 wild type littermates. The results from this study demonstrated the presence of several genetic modifiers of nicotine consumption in Chrna5 KO mice as well as identify loci that may affect nicotine consumption independent of Chrna5 genotype.

(Frontiers in Psychiatry, 2021)

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