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Retrieved January 8, Edmonton Sun. Calgary Herald. December 11, Entertainment Weekly. Archived from the original on November 5, Retrieved January 18, Online Film Critics Society. Archived from the original on January 21, Retrieved January 15, Archived from the original on April 15, Guadalajara International Film Festival.
Archived from the original on January 24, Retrieved January 17, Archived from the original on January 28, Retrieved December 3, International Press Academy. Archived from the original on May 22, Archived from the original on February 10, Retrieved December 2, July 15, Archived PDF from the original on January 21, Retrieved January 15, — via Deadline Hollywood. Paramount Network. Archived from the original on October 23, Retrieved January 27, Archived from the original on January 3, Retrieved December 20, Archived from the original on December 11, Finally, nicotine enhanced ethanol-induced hypothermia but decreased ethanol intake in the DID test.
Conclusion Our results demonstrate that nicotine synergistically enhances ethanol-induced LORR in the mouse. Keywords: ethanol, nicotine, mice, LORR Introduction Ethanol abuse and nicotine use are two leading causes of preventable mortality in the world. Ethanol abuse is responsible for nearly 80, deaths each year in the United States while tobacco products are responsible for nearly , deaths each year in the United States Centers for Disease Control This high co-morbidity of use increases the difficulty of achieving long-term abstinence with either drug Larsson et al.
Current evidence strongly points to the existence of complex biological interactions between the drugs, which suggests that there may be common biological mechanisms mediating co-abuse True et al. Additionally, there is evidence of both synergistic and antagonistic interactions between the two drugs. For example, exposure to ethanol and nicotine together results in additive dopamine release in the nucleus accumbens of rats Schlaepfer et al. In contrast, nicotine attenuates ethanol-induced ataxia Taslim et al.
Mecamylamine, a nonselective antagonist of nicotinic acetylcholine receptors nAChRs , has been shown to decrease ethanol-induced dopaminergic neuron activation and ethanol intake in mice Hendrickson et al. Furthermore, the development of cross-tolerance between nicotine and ethanol has also been observed Collins et al.
The initial response to a drug is likely to be one factor contributing to the risk for future abuse or dependence de Wit and Phillips Indeed, work by Schuckit et al. Individuals that are relatively insensitive to the effects of ethanol low level of response are relatively more susceptible to developing alcohol use disorders.
In contrast, increased sensitivity to the unpleasant subjective effects of intoxication, such as ataxia and sedation, has been posited to serve as a protective influence by discouraging drinking Krystal et al. Similarly, higher ethanol consuming lines of mice are less sensitive to the sedative-hypnotic and ataxic effects of ethanol Shen et al.
Preclinical data have suggested that nicotine may initially reduce the aversive effects of ethanol. For example, nicotine reverses ethanol-induced cognitive impairments and conditioned taste aversion in rodents Kunin et al. We therefore hypothesized that nicotine would decrease the duration of the loss of righting reflex LORR , a common measure of ethanol's sedative-hypnotic effects.
The purpose of the present experiments was to examine the effects of nicotine administration on the duration of ethanol-induced LORR and to characterize their pharmacological interactions in mice through dose-response, receptor efficacy, strain difference and tolerance measures. We also evaluated the involvement of major nAChR subtypes in mediating the effects of nicotine on ethanol sedation. To understand if the effect of nicotine on ethanol extended to other behaviors, we investigated the impact of nicotine on ethanol intake in the DID paradigm and ethanol-induced hypothermia as well.
John Drago Ross et al. Mutant strains were maintained as heterozygotes; experimental animals were obtained from crossing heterozygote mice to generate mutant and wild-type littermates. All experiments were performed on male mice. Mice were 8—10 weeks of age and weighed approximately 25—30 g at the start of each experiment. All experiments were performed during the normal light cycle between a.
All studies were carried out in accordance with the National Institute of Health guide for the Care and Use of Laboratory animals. Ketamine HCl was purchased from Vedco Inc. Saint Joseph, MO. These drugs were dissolved in 0. Ethanol was also dissolved in 0.
All doses are expressed as the free base of the drug. We generated an ethanol dose response curve by injecting mice with varying doses of ethanol 2. In establishing a dose response curve for nicotine plus ethanol, mice were injected with varying doses of nicotine 0.
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