Modulation of ethanol drinking-in-the-dark by mecamylamine and nicotinic acetylcholine receptor agonists in C57BL/6J mice

@article{Hendrickson2009ModulationOE,
  title={Modulation of ethanol drinking-in-the-dark by mecamylamine and nicotinic acetylcholine receptor agonists in C57BL/6J mice},
  author={Linzy M. Hendrickson and Rubing Zhao-Shea and Andrew R. Tapper},
  journal={Psychopharmacology},
  year={2009},
  volume={204},
  pages={563-572}
}
RationaleRecent reports describe a restricted access ethanol consumption paradigm where C57Bl/6J mice drink until intoxicated. Termed “drinking in the dark” (DID), this paradigm has been used as a model of binge drinking. Although neuronal nicotinic acetylcholine receptors (nAChRs) have been implicated in alcohol drinking in rats pre-trained to self-administer ethanol, their role in binge-like ethanol consumption is unknown.ObjectivesTo determine if nAChRs are involved in binge drinking as… Expand
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TLDR
Evidence is provided that α7 nAChRs are involved in ethanol consumption and supports the idea that pharmacological manipulation of nA ChRs reduces ethanol intake, and there may be functional redundancy in the nicotinic control of alcohol drinking. Expand
Neuronal nicotinic receptor ligands modulate chronic nicotine-induced ethanol consumption in C57BL/6J mice
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Results indicate that nAChRmediated signaling is critical in regulating nicotine-induced ethanol drinking behaviors, and indicates that neuronal nicotinic acetylcholine receptors in the midbrain dopamine system are common targets for the neurobehavioral interactions between alcohol and nicotine. Expand
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TLDR
It is found that sazetidine-A enhances alcohol aversion without affecting the expression or acquisition of conditioned alcohol reward in C57BL/6J mice, and a previously unknown role for non- α4 containing nAChRs in alcohol aversion is identified. Expand
Exposure to nicotine increases nicotinic acetylcholine receptor density in the reward pathway and binge ethanol consumption in C57BL/6J adolescent female mice
TLDR
Data show that nicotine exposure during adolescence increases subsequent binge ethanol consumption, and may affect the number of nAChRs in regions of the brain reward pathway, specifically the frontal cortex, in mice exposed to nicotine and ethanol. Expand
Lobeline and cytisine reduce voluntary ethanol drinking behavior in male C57BL/6J mice
  • Ravi K Sajja, S. Rahman
  • Chemistry, Medicine
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry
  • 2011
TLDR
Findings provide evidence that nAChR-mediated signaling plays a critical role in ethanol drinking behavior in mice and nicotinic ligands have therapeutic potential for cessation of binge-like ethanol drinking and dependence in humans. Expand
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TLDR
It is concluded that β2* nAChRs, along with being key components in nicotine dependence, may also present viable candidates in the discovery of the molecular underpinnings of alcohol dependence. Expand
Nicotinic receptor ligands reduce ethanol intake by high alcohol-drinking HAD-2 rats.
TLDR
Findings provide further evidence that activity at the nAChR influences ethanol intake and is a promising target for pharmacotherapy development for the treatment of alcohol dependence and relapse. Expand
THE ROLE OF NICOTINIC ACETYLCHOLINE RECEPTORS IN ETHANOL RESPONSIVE BEHAVIORS AND DRINKING
THE ROLE OF NICOTINIC ACETYLCHOLINE RECEPTORS IN ETHANOL RESPONSIVE BEHAVIORS AND DRINKING By Anton Jerome Dawson, B.S., B.A. A Dissertation submitted in partial fulfillment of the requirements for… Expand
Enhancement of alcohol aversion by the nicotinic acetylcholine receptor drug sazetidine‐A
TLDR
It is found that sazetidine‐A enhances the expression of alcohol aversion, which may underlie the reduction in alcohol consumption induced by sazetic acid, and elucidating the identity of non‐α4 nAChRs in alcohol aversion mechanisms will provide a better understanding of the complex role of nAR agonists in alcohol addiction. Expand
Inhibitory influence of mecamylamine on the development and the expression of ethanol-induced locomotor sensitization in mice
TLDR
The hypothesis that neuroadaptive changes in nAChRs may participate in the development and the expression of ethanol-induced locomotor sensitization is supported. Expand
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