Alcoholism is characterized by increased ethanol intake, loss of control over ethanol intake, and compulsive ethanol taking. Progress in understanding the neurobiological basis of excessive ethanol drinking depends on the combined development and use of molecular and neuropharmacological tools for understanding the mechanisms of ethanol actions and animal models that allow interpretation of these advances in the context of ethanol addiction. The primary goal of the Mouse Animal Models Core is to provide well characterized and validated behavioral models of excessive ethanol consumption to INIA investigators. This Core has been completely designed around the specific needs of the INIA-West group and has developed from intense discussions and contact with everyone. Inherent in the goal of the Core is that it allows for both the standardization of these models and the pooling of resources. This Core will service twelve INIA investigators studying each of the two domains (Binge and Dependence, see below) and their three levels of analysis (neurocircuitry, cellular, and molecular). In this way, the Core shares the responsibility of making this consortium highly integrated and multidisciplinary and establishes economies of scale. Individual laboratories can focus on their own expertise and will not be required to establish these models in their own laboratories. One of the most innovative aspects of this Core is the application of its neuroadaptive models to the many genetic models (transgenics, knockouts, selectively bred mice) being studied and/or produced by INIA investigators. This will allow for a comprehensive study of the combined impact of genes and environment on the process of ethanol addiction and represents a major strength of the present application. In addition, these models will be extended to additional strains such as those used in the production of knockout and transgenic strains and those commonly used in ethanol research. Finally, this Core will examine phenotypic correlates of excessive alcohol consumption as this is critical to both our understanding of the susceptibility. Based on INIA investigators' needs the following Specific Aims have been formulated:
Specific Aim 1. To provide established and refined neuroadaptive models to INIA investigators and Specific Aim 2. To combine neuroadaptive models with genetic models for INIA investigators. ? ? ?
| Harris, R Adron; Bajo, Michal; Bell, Richard L et al. (2017) Genetic and Pharmacologic Manipulation of TLR4 Has Minimal Impact on Ethanol Consumption in Rodents. J Neurosci 37:1139-1155 |
| Bajo, Michal; Varodayan, Florence P; Madamba, Samuel G et al. (2015) IL-1 interacts with ethanol effects on GABAergic transmission in the mouse central amygdala. Front Pharmacol 6:49 |
| Herman, Melissa A; Sidhu, Harpreet; Stouffer, David G et al. (2015) GIRK3 gates activation of the mesolimbic dopaminergic pathway by ethanol. Proc Natl Acad Sci U S A 112:7091-6 |
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| Repunte-Canonigo, Vez; Chen, Jihuan; Lefebvre, Celine et al. (2014) MeCP2 regulates ethanol sensitivity and intake. Addict Biol 19:791-9 |
| Hauser, Sheketha R; Hedlund, Peter B; Roberts, Amanda J et al. (2014) The 5-HT7 receptor as a potential target for treating drug and alcohol abuse. Front Neurosci 8:448 |
| Trujillo, Jennifer L; Do, David T; Grahame, Nicholas J et al. (2011) Ethanol consumption in mice: relationships with circadian period and entrainment. Alcohol 45:147-59 |
| Repunte-Canonigo, Vez; van der Stap, Lena D; Chen, Jihuan et al. (2010) Genome-wide gene expression analysis identifies K-ras as a regulator of alcohol intake. Brain Res 1339:1-10 |
| Repunte-Canonigo, Vez; Berton, Fulvia; Cottone, Pietro et al. (2010) A potential role for adiponectin receptor 2 (AdipoR2) in the regulation of alcohol intake. Brain Res 1339:11-7 |
| Trujillo, Jennifer L; Roberts, Amanda J; Gorman, Michael R (2009) Circadian timing of ethanol exposure exerts enduring effects on subsequent ad libitum consumption in C57 mice. Alcohol Clin Exp Res 33:1286-93 |
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