Gustatory, Trigeminal, and Olfactory Aspects of Nicotine Intake in Three Mouse Strains

Gyekis, Joseph P.; Dingman, Marc A.; Revitsky, Alicia R.; Bryant, Bruce P.; Vandenbergh, David J.; Frank, Marion E.; Blizard, David A.

doi:10.1007/s10519-012-9546-x

Cited by 19 publications

(14 citation statements)

References 73 publications

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“…Some compounds, such as nicotine, may possess additional sensory properties, such as olfactory or trigeminal components for rodents [ 38 ]. The sensory properties of the tested ligands have not yet been established for chickens, but the fact that in-vivo threshold is equal or higher than the in-vitro ggTas2r threshold, suggests that the potential additional sensory properties do not dominate the aversion effect.…”

Section: Discussionmentioning

confidence: 99%

From Cell to Beak: In-Vitro and In-Vivo Characterization of Chicken Bitter Taste Thresholds

et al. 2017

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Bitter taste elicits an aversive reaction, and is believed to protect against consuming poisons. Bitter molecules are detected by the Tas2r family of G-protein-coupled receptors, with a species-dependent number of subtypes. Chickens demonstrate bitter taste sensitivity despite having only three bitter taste receptors—ggTas2r1, ggTas2r2 and ggTas2r7. This minimalistic bitter taste system in chickens was used to determine relationships between in-vitro (measured in heterologous systems) and in-vivo (behavioral) detection thresholds. ggTas2r-selective ligands, nicotine (ggTas2r1), caffeine (ggTas2r2), erythromycin and (+)-catechin (ggTas2r7), and the Tas2r-promiscuous ligand quinine (all three ggTas2rs) were studied. Ligands of the same receptor had different in-vivo:in-vitro ratios, and the ggTas2r-promiscuous ligand did not exhibit lower in-vivo:in-vitro ratios than ggTas2r-selective ligands. In-vivo thresholds were similar or up to two orders of magnitude higher than the in-vitro ones.

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Section: Discussionmentioning

confidence: 99%

From Cell to Beak: In-Vitro and In-Vivo Characterization of Chicken Bitter Taste Thresholds

et al. 2017

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“…Genetic differences that impact taste perception may impact oral nicotine preference (Gyekis et al, 2012). Because we were unable to find data in the literature for the tastant preference in the MT 1 /MT 2 double-null mutant animals, we tested their preference for the bitter quinine solution and the sweet tastant saccharin.…”

Section: Resultsmentioning

confidence: 99%

“…Previous work has shown that differences in nicotine preference drinking between inbred mouse strains are at least partially due to differences in taste preferences (Dahl et al, 1997). Furthermore, Gyekis et al showed that mice that have been conditioned to avoid a bitter tasting quinine solution will also transfer this conditioning to nicotine solutions, and vice versa (Gyekis et al, 2012). This suggests that some portion of the sensory experience of nicotine is bitter tasting, and it could be possible that melatonin receptors play some role in bitter taste, but not in the rewarding properties of nicotine itself.…”

Section: Discussionmentioning

confidence: 99%

Melatonin administration alters nicotine preference consumption via signaling through high-affinity melatonin receptors

et al. 2015

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Rationale While it is known that tobacco use varies across the 24-hour day, the time-of-day effects are poorly understood. Findings from several previous studies indicate a potential role for melatonin in these time-of-day effects; however the specific underlying mechanisms have not been well characterized. Understanding of these mechanisms may lead to potential novel smoking cessation treatments. Objective Examine the role of melatonin and melatonin receptors in nicotine free choice consumption Methods A two-bottle oral nicotine choice paradigm was utilized with melatonin supplementation in melatonin deficient mice (C57BL/6J) or without melatonin supplementation in mice proficient at melatonin synthesis (C3H/Ibg) compared to melatonin proficient mice lacking both or one of the high affinity melatonin receptors (MT1 and MT2; double null mutant DM, or MT1 or MT2). Preference for bitter and sweet tastants also was assessed in wild type and MT1 and MT2 DM mice. Finally, home cage locomotor monitoring was performed to determine the effect of melatonin administration on activity patterns. Results Supplemental melatonin in drinking water significantly reduced free-choice nicotine consumption in C57BL/6J mice, which do not produce endogenous melatonin, while not altering activity patterns. Independently, genetic deletion of both MT1 and MT2 receptors in a melatonin proficient mouse strain (C3H) resulted in significantly more nicotine consumption than controls. However single genetic deletion of either the MT1 or MT2 receptor alone did not result in increased nicotine consumption. Deletion of MT1 and MT2 did not impact taste preference. Conclusions This study demonstrates that nicotine consumption can be affected by exogenous or endogenous melatonin and requires at least one of the high-affinity melatonin receptors. The fact that expression of either the MT1 or MT2 melatonin receptor is sufficient to maintain lower nicotine consumption suggests functional overlap and potential mechanistic explanations. Keywords: Melatonin, Nicotine, Mice, Preference Drinking

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“…While these paradigms have been successful in getting rats to self-administer both drugs, in some cases at pharmacologically relevant levels (Hauser, Katner, et al, 2012), the results obtained relating these two drugs may in some cases be determined by their specific properties or the specific paradigms of administration. When given orally, both substances have orosensory properties that include a bitter taste, aversive odor, or irritating effect (Gyekis et al, 2012; Oliveira-Maia et al, 2009; Thuerauf et al, 2000) which by themselves may influence drug-taking behavior (Crabbe, Harris, & Koob, 2011; Gyekis et al, 2012; Kulkosky, 1985). Also, a specific paradigm involving sequential administration of the two drugs may yield results reflecting the effect of one drug on intake of the other, rather than the co-use of these drugs.…”

Section: Discussionmentioning

confidence: 99%

“…First, we tested a new paradigm which involves IV self-administration of both nicotine and ethanol, separately and together, and permits us to examine changes in their co-use while avoiding certain aversive properties and interactions associated with oral self-administration of ethanol as well as nicotine (Gyekis et al, 2012; Kiefer & Dopp, 1989; Oliveira-Maia et al, 2009; Thuerauf, Kaegler, Renner, Barocka, & Kobal, 2000). Second, with this paradigm that allowed significant simultaneous IV self-administration, we then examined the effect of maternal consumption of a fat-rich diet, during gestation and lactation, on different aspects of nicotine/ethanol self-administration behavior in the offspring.…”

Section: Introductionmentioning

confidence: 99%

Nicotine and ethanol co-use in Long-Evans rats: Stimulatory effects of perinatal exposure to a fat-rich diet

Karatayev

Lukatskaya

Moon

et al. 2015

Alcohol

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Clinical studies demonstrate frequent co-existence of nicotine and alcohol abuse and suggest that this may result, in part, from the ready access to and intake of fat-rich diets. Whereas animal studies show that high-fat diet intake in adults can enhance the consumption of either nicotine or ethanol and that maternal consumption of a fat-rich diet during pregnancy increases operant responding for nicotine in offspring, little is known about the impact of dietary fat on the co-abuse of these two drugs. The goal of this study was to test in Long-Evans rats the effects of perinatal exposure to fat on the co-use of nicotine and ethanol, using a novel paradigm that involves simultaneous intravenous (IV) self-administration of these two drugs. Fat- vs. chow-exposed offspring were characterized and compared, first in terms of their nicotine self-administration behavior, then in terms of their nicotine/ethanol self-administration behavior, and lastly in terms of their self-administration of ethanol in the absence of nicotine. The results demonstrate that maternal consumption of fat compared to low-fat chow during gestation and lactation significantly stimulates nicotine self-administration during fixed-ratio testing. It also increases nicotine/ethanol self-administration during fixed-ratio and dose-response testing, with BEC elevated to 120 mg/dL, and causes an increase in breakpoint during progressive ratio testing. Of particular note is the finding that rats perinatally exposed to fat self-administer significantly more of the nicotine/ethanol mixture as compared to nicotine alone, an effect not evident in the chow-control rats. After removal of nicotine from the nicotine/ethanol mixture, this difference between the fat- and chow-exposed rats was lost, with both groups failing to acquire the self-administration of ethanol alone. Together, these findings suggest that perinatal exposure to a fat-rich diet, in addition to stimulating self-administration of nicotine, causes an even greater vulnerability to the excessive co-use of nicotine and ethanol.

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Gustatory, Trigeminal, and Olfactory Aspects of Nicotine Intake in Three Mouse Strains

Cited by 19 publications

References 73 publications

From Cell to Beak: In-Vitro and In-Vivo Characterization of Chicken Bitter Taste Thresholds

From Cell to Beak: In-Vitro and In-Vivo Characterization of Chicken Bitter Taste Thresholds

Melatonin administration alters nicotine preference consumption via signaling through high-affinity melatonin receptors

Nicotine and ethanol co-use in Long-Evans rats: Stimulatory effects of perinatal exposure to a fat-rich diet

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