This dissertation presents three separate studies designed to provide structure and evidence-based insight into the characteristics associated with responsible drinking. First, a primer on the responsible drinking message will be presented discussing: (a) the origins and evolution of this message, (b) alcohol product advertisements evincing a responsible drinking prevention message, and (c) practical and ethical concerns associated with brewer-sponsored responsible drinking campaigns. Additionally, the primer will also present systematic reviews of twenty (n=20) empirical studies utilizing the responsible drinking concept to determine the manner in which researchers currently conceptualize and explain characteristics of responsible drinking in their reports. Secondly, a qualitative examination of college students’ beliefs, motivations, intentions, and behaviors regarding responsible drinking will be presented. Employing an emergent design, the data collection process encompassed four focus group sessions and three separate, personal interviews. The final sample size comprised thirteen individuals (Focus Group n=10; Personal Interview n=3). A conceptual model will also be proposed to assist in interpreting the qualitative findings and theorizing about factors influencing intentions to drink responsibly. Lastly, drawing upon the theoretical model and qualitative findings, the development and rigorous psychometric testing of a web-based instrument - Characteristics of Responsible Drinking Survey (CHORDS) – will be discussed. Zoomerang™ served as the host-site for both the pilot- and final testing phases of the CHORDS. The final sample (n=729) comprised a random set of individuals drawn from all currently enrolled students (undergraduate and graduate) attending Texas A&M University (TAMU) in College Station. Principal components exploratory factor analysis revealed the CHORDS consists of five scales (61 total items) whose scores exhibit high internal consistency reliability. These scales include: Behavioral Beliefs, Motivation, Self-Efficacy, Barriers and Behavioral Intention. Scales were found to measure the same underlying construct, as outlined in the theoretical model. Prior to this study, scientific literature contained no scholarly attempts to distinguish responsible drinking characteristics; no theoretically-based explanation or examination of the interactions among responsible drinking variables; and no instruments expressly intended to measure responsible drinking intentions. Thus, this study represents the first step toward addressing the limitations associated with responsible drinking and filling the apparent conceptual gaps.

Expectancies about the effects of alcohol predict alcohol consumption among adolescent children. Although alcohol-expectancy measures have been validated to use with English speaking populations, there is currently no available information on the psychometric properties of the Comprehensive Effects of Alcohol (CEOA) questionnaire with Spanish speaking populations. Using confirmatory factor analysis (CFA), the factor structure of the Spanish version of the CEOA was assessed in a set of scores obtained from a sample of adolescents from Mexico (N = 345). The results replicated the 7-factor structure of the CEOA. Moreover, CEOA factor-scale derived scores predicted alcohol use. Overall, the CEOA-Spanish appears to be a valid measure of alcohol expectancies for use with Mexican adolescents.

Thesis (Ph. D.)--Rutgers University, 2009. / "Graduate Program in Neuroscience." Includes bibliographical references (p. 52-60).

Thesis (Ph. D.)--University of Texas at Austin, 2002. / Vita. Includes bibliographical references. Available also from UMI Company.

Thesis (Ph. D.)--University of Texas at Austin, 2003. / Vita. Includes bibliographical references. Available also from UMI Company.

Thesis (Ph. D.)--Ohio State University, 2004. / Title from first page of PDF file. Document formatted into pages; contains xxxiii, 278 p.; also includes graphics. Includes abstract and vita. Advisor: Kenneth Chan, Dept. of Pharmacy. Includes bibliographical references (p. 266-278).

Synaptic alterations in the nucleus accumbens (NAc) are crucial for the aberrant reward-associated learning that forms the foundation of drug dependence. Glutamatergic synaptic plasticity in the NAc has been implicated in several behavioral responses to psychomotor stimulating agents, such as cocaine and amphetamine, yet no studies, at present, have investigated its modulation by ethanol. We demonstrated that both in vitro and in vivo ethanol treatment significantly disrupts normal synaptic functioning in medium spiny neurons (MSNs) of the NAc shell. Utilizing whole-cell voltage clamp recording techniques, synaptic conditioning (low frequency stimulation with concurrent postsynaptic depolarization) reliably depressed (NAc-LTD) AMPA-mediated excitatory postsynaptic currents (EPSCs). Acute ethanol exposure inhibited the depression of AMPA EPSCs differentially with increasing concentrations, but this inhibitory action of ethanol was reversed by a D1-like dopamine receptor agonist. When examined 24 hours following a single bout of in vivo chronic intermittent ethanol (CIE) vapor exposure, NAc-LTD was absent and instead synaptic potentiation (LTP) was reliably observed. We further investigated CIE-induced modulation of NAc-LTD by distinguishing between the two subpopulations of MSNs in the NAc, D1 receptor-expressing (D1+) and D2 receptor-expressing (D1-). We determined that NAc-LTD is expressed solely in D1+ but not D1- MSNs. In addition, 24 hours following a repeated regimen of in vivo CIE exposure NAc-LTD is completely occluded in D1+ MSNs, while D1- MSNs are able to express LTD. Complete recovery of normal synaptic plasticity expression in both D1+ and D1- MSNs does not occur until two weeks of withdrawal from CIE vapor exposure. To our knowledge, this is the first demonstration of a reversal in the cell type-specificity of synaptic plasticity in the NAc shell, as well as, the gradual recovery of the pre-drug exposure plasticity state following extended withdrawal. This study suggests that NAc-LTD is cell type-specific and highly sensitive to both acute and chronic ethanol exposure. We believe these observations also highlight the adaptability of NAc MSNs to the effects of long-term ethanol exposure. A change in these synaptic processes may constitute a neural adaptation that contributes to the induction and/or expression of alcohol dependence. / text

Alcohol abuse is an enormous problem causing death and disability to over 43 million people worldwide each year (WHO). Chronic alcohol consumption also contributes to abnormal brain morphology and significant brain volume loss indicative of neurodegeneration. Until there are effective treatments to alter maladaptive behavioral patterns in alcohol abuse, more research is needed to prevent alcohol-induced toxicity and degeneration. We used C. elegans as a model system to identify genetic modulators of alcohol toxicity and explored whether prolonged alcohol exposure damages the nervous system. In our study, we exposed L4-larval stage worms to varying concentrations of ethanol for three days and found a dose-dependent deficit in crawling. Furthermore, we evaluated degeneration by assessing the health of neurons using fluorescent reporters. Compared to the untreated group, we found that ethanol-exposed worms had a significant neurodegeneration. Previous findings using C. elegans have suggested that the innate immune pathway may protect against neurodegeneration caused by drug toxicity (Schreiber & McIntire, 2012). We find that deletion of either the innate immune gene nsy-1 (orthologous to the mammalian ASK-1 MAPKKK) or pmk-1 (orthologous to the mammalian p38 MAPK) caused hypersensitivity to ethanol toxicity. Conversely, boosting innate immune signaling via gain-of-function mutation in nsy-1 produced resistance to ethanol toxicity and ameliorated ethanol-induced cholinergic degeneration. Our findings indicate that prolonged exposure to ethanol leads to both behavioral impairments and neuronal degeneration in C. elegans and that the ASK1/p38 MAP kinase pathway may play a role in ethanol-induced damage to the nervous system. / text

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