Studies of nicotine consumption in rodents often intend to investigate nicotine's post-absorptive effects, yet little is known about the pre-absorptive sensory experience of nicotine drinking, including gustatory, trigeminal, and olfactory influences. We conditioned taste aversion (CTA) to nicotine in males of 3 inbred mouse strains: C57BL/6J, DBA/2J, and 129X1/SvJ by repeatedly pairing 150 μg/ml nicotine drinking with lithium chloride injections. Generalization to a variety of bitter, sour, sweet, salty, and irritant solutions and to nicotine odor was then examined. Nicotine CTA generalized to the bitter stimulus quinine hydrochloride and the chemosensory irritant spilanthol in all strains. It also showed strain specificity, generalizing to hydrogen peroxide (an activator of TRPA1) in C57BL/6J mice and to the olfactory cue of nicotine in DBA/2J mice. These behavioral assays demonstrate that the sensory properties of nicotine are complex and include multiple gustatory, irritant, and olfactory components. How these qualities combine at the level of perception remains to be assessed, but sensory factors clearly exert an important influence on nicotine ingestion and their contribution to net intake of nicotine should not be neglected in animal or human studies.

Ghrelin is a gut-brain hormone that regulates energy balance through food consumption. While ghrelin is well known for its role in hypothalamic activation and homeostatic feeding, more recent evidence suggests that ghrelin also is involved in hedonic feeding through the dopaminergic reward pathway. This paper investigated how ghrelin administration (intraperitoneal, intracerebroventricular, or directly into dopaminergic reward-relevant brain regions) activates the dopaminergic reward pathway and associated reward-relevant behavioral responses in rodents. A total of 19 empirical publications that examined one or more of these variables were included in this review. Overall, ghrelin administration increases dopamine levels in the nucleus accumbens, as well as reward-relevant behaviors such as food (both standard chow and palatable foods) and alcohol consumption. Ghrelin administration also increases operant responding for sucrose, and conditioned place preference. Following a review of the small body of literature examining the effects of ghrelin administration on the dopamine reward pathway, we present a model of the relationship between ghrelin and dopaminergic reward activation. Specifically, ghrelin acts on ghrelin receptors (GHS-R1A) in the ventral tegmental area (VTA) and lateral dorsal tegmental nucleus (LDTg) to stimulate the mesolimbic dopamine reward pathway, which results in increased rewarding behaviors in rodents. Results from this review suggest that selective antagonism of the ghrelin system may serve as potential treatment for addictive drug use. This review highlights gaps in the literature, including a lack of examination of sex- or age-related differences in the effects of ghrelin on dopamine reward processes. In light of vulnerability to drug abuse among female and adolescent populations, future studies should target these individual difference factors.

Background : Individuals with disordered eating have the highest mortality rate of any psychiatric disorder and females make up the majority of the eating disordered population . Tobacco smokers have lower BMIs than do their non-smoking counterparts, and adolescent and adult females report using tobacco to lose or maintain body weight. Multiple biobehavioural factors contribute to this nicotine-body weight relationship, rodent studies suggest that reduced food intake following nicotine exposure may be a primary factor. Objective : To examine the effects of nicotine on body weight changes in response to different food types. Methods : We used an oral nicotine administration paradigm to investigate body weight changes in the presence of standard chow, high sweet and high fat foods in adolescent (N=63) and adult (N=60) female C57BL/6J mice. Mice were exposed to nicotine (200 µg/ml) or water along with one of three food types for 7 days. Results : Adult mice weighed more but ate less food than did adolescents (p < 0.05). Mice exposed to high fat food weighed the most, but ate the least (p < 0.05). While there were no main effects of nicotine on body weight in either age group, nicotine-exposed adults consumed less food than did water-exposed adults (p < 0.05), this effect was not seen in adolescents. Among the nicotine-exposed mice, adolescents consumed more food than did adults (p < 0.05). Conclusions : These findings suggest, in females, the appetite suppression qualities of nicotine differ based on age, with nicotine exposure actually increasing food consumption in adolescents. Nicotine's effects on food intake do not result in body weight changes in either age group