Search

Alcohol is one of the most prevalent addictive substances in the world. Withdrawal symptoms result from abrupt cessation of alcohol consumption in habitual drinkers. The emergence of both affective and physical symptoms produces a state that promotes relapse. Mice provide a preclinical model that could be used to study alcohol dependence and withdrawal while controlling for both genetic and environmental variables. The use of a liquid ethanol diet offers a reliable method for the induction of alcohol dependence in mice, but this approach is impractical when conducting high-throughput pharmacological screens or when comparing multiple strains of genetically engineered mice. The goal of this study was to compare withdrawal-associated behaviors in mice chronically treated with a liquid ethanol diet vs. mice treated with a short-term ethanol treatment that consisted of daily ethanol injections containing the alcohol dehydrogenase inhibitor, 4-methylpyrazole. Twenty-four hours after ethanol treatment, mice were tested in the open field arena, the elevated plus maze, the marble burying test, or for changes in somatic signs during spontaneous ethanol withdrawal. Anxiety-like and compulsive-like behaviors, as well as physical signs, were all significantly elevated in mice undergoing withdrawal, regardless of the route of ethanol administration. Therefore, a short-term ethanol treatment can be utilized as a screening tool for testing genetic and pharmacological agents before investing in a more time-consuming ethanol treatment. [ABSTRACT FROM AUTHOR]

Nicotine dependence plays a critical role in addiction to tobacco products, and thus contributes to a variety of devastating tobacco-related diseases (SGR 2014). Annual costs associated with smoking in the US are estimated to be between $289 and $333 billion. Effective interventions for nicotine dependence, especially in smokers, are a critical barrier to the eradication of tobacco-related diseases. This overview highlights research presented at the Plenary Symposium of Behavior, Biology and Chemistry: Translational Research in Addiction Conference (BBC), hosted by the UT Health Science Center San Antonio, on March 9-10, 2013. The Plenary Symposium focused on tobacco addiction, and covered topics ranging from basic science to national policy. As in previous years, the meeting brought together globally-renowned scientists, graduate student recruits, and young scientists from underrepresented populations in Texas and other states with the goal of fostering interest in drug addiction research in young generations. [ABSTRACT FROM AUTHOR]

Abstract: Nicotine dependence plays a critical role in addiction to tobacco products, and thus contributes to a variety of devastating tobacco-related diseases (SGR 2014). Annual costs associated with smoking in the US are estimated to be between $289 and $333 billion. Effective interventions for nicotine dependence, especially in smokers, are a critical barrier to the eradication of tobacco-related diseases. This overview highlights research presented at the Plenary Symposium of Behavior, Biology and Chemistry: Translational Research in Addiction Conference (BBC), hosted by the UT Health Science Center San Antonio, on March 9–10, 2013. The Plenary Symposium focused on tobacco addiction, and covered topics ranging from basic science to national policy. As in previous years, the meeting brought together globally-renowned scientists, graduate student recruits, and young scientists from underrepresented populations in Texas and other states with the goal of fostering interest in drug addiction research in young generations. [Copyright &y& Elsevier]

The nicotinic acetylcholine receptor (nAChR) is a receptor, ion channel complex composed of five polypeptide subunits. There are many different nAChR subtypes constructed from a variety of different subunit combinations. This structural diversity contributes to the varied roles of nAChRs in the peripheral and central nervous system, and this diversity offers an excellent opportunity for chemists who are producing ligands. Subunit specific ligands could have wide and varied effects in the laboratory as experimental tools and in the clinic as therapeutic agents. Because presynaptic nAChRs have been shown to enhance the release of many neurotransmitters, new nicotinic ligands that potentiate nAChR activity would be very useful. Such ligands could enhance the release of various neurotransmitters during degenerative diseases that cause neurotransmitter systems to decrease their output. For example, boosting the release from cholinergic neurons would help patients with Alzheimer''s disease, and boosting the release from dopaminergic neurons would help patients with Parkinson''s disease. [Copyright &y& Elsevier]

Diseases associated with tobacco use constitute a major health problem worldwide. Upon cessation of tobacco use, an unpleasant withdrawal syndrome occurs in dependent individuals. Avoidance of the negative state produced by nicotine withdrawal represents a motivational component that promotes continued tobacco use and relapse after smoking cessation. With the modest success rate of currently available smoking cessation therapies, understanding mechanisms involved in the nicotine withdrawal syndrome are crucial for developing successful treatments. Animal models provide a useful tool for examining neuroadaptative mechanisms and factors influencing nicotine withdrawal, including sex, age, and genetic factors. Such research has also identified an important role for nicotinic receptor subtypes in different aspects of the nicotine withdrawal syndrome (e.g., physical vs. affective signs). In addition to nicotinic receptors, the opioid and endocannabinoid systems, various signal transduction pathways, neurotransmitters, and neuropeptides have been implicated in the nicotine withdrawal syndrome. Animal studies have informed human studies of genetic variants and potential targets for smoking cessation therapies. Overall, the available literature indicates that the nicotine withdrawal syndrome is complex, and involves a range of neurobiological mechanisms. As research in nicotine withdrawal progresses, new pharmacological options for smokers attempting to quit can be identified, and treatments with fewer side effects that are better tailored to the unique characteristics of patients may become available. This article is part of the Special Issue entitled ‘The Nicotinic Acetylcholine Receptor: From Molecular Biology to Cognition’. [ABSTRACT FROM AUTHOR]