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Dickson, P. E.

Publications and source records attributed to Dickson, P. E..

2 recordsLinked to original sources

Discovery of a role for Rab3b in habituation and cocaine induced locomotor activation in mice using heterogeneous functional genomic analysis

Substance use disorders are prevalent and present a tremendous societal cost but the mechanisms underlying addiction behavior are poorly understood and few biological treatments exist. One strategy to identify novel molecular mechanisms of addiction is through functional genomic experimentation. However, results from individual experiments are often noisy. To address this problem, the convergent analysis of multiple genomic experiments can prioritize signal from these studies. In the present study, we examine genetic loci identified in the recombinant inbred (BXD RI) genetic reference population that modulate the locomotor response to cocaine. We then applied the GeneWeaver software system for heterogeneous functional genomic analysis to integrate and aggregate multiple studies of addiction genomics, resulting in the identification of Rab3b, as a functional correlate of the locomotor response to cocaine in rodents. This gene encodes a member of the RAB family of Ras-like GTPases known to be involved in trafficking of secretory and endocytic vesicles in eukaryotic cells. The convergent evidence for a role of Rab3b was included co-occurrence in previously published genetic mapping studies of cocaine related behaviors; methamphetamine response and Cartpt (Cocaine- and amphetamine-regulated transcript prepropeptide) abundance; evidence related to other addictive substances; density of polymorphisms; and its expression pattern in reward pathways. To evaluate this finding, we examined the effect of RAB3 complex perturbation in cocaine response. B6;129-Rab3btm1Sud Rab3ctm1sud Rab3dtm1sud triple null mice (Rab3bcd-/-) exhibited significant deficits in habituation, and increased acute and repeated cocaine responses. This previously unidentified mechanism of the behavioral predisposition and response to cocaine is an example of many that can be identified and validated using aggregate genomic studies. Many genetic and genomic studies have been performed over the past few decades, representing a wealth of data on the underlying neurobiological and genetic basis of multiple complex behaviors. However, these studies, particularly legacy studies using older technologies and resources lack precision. By aggregating multiple studies, convergent evidence for shared molecular mechanisms of multiple behaviors can be found, for example the widely reported relations among psychostimulant use and novelty response behavior. Here a legacy genetic mapping result for a cocaine related trait mapped in mice was refined using data from 113 different experimental gene sets related to addiction in the GeneWeaver system for heterogeneous functional genomic analysis. Convergent evidence revealed a role for Rab3b in this and other traits including multiple psychostimulant responses and CART expression. Experimental perturbation of the RAB complex revealed effects on habituation to a novel environment, cocaine induced activation and Carpt expression. The analysis of aggregate data thus revealed a molecular mechanism that influences the relationship between response to novel situations and cocaine-related phenotypes.

neuroscience

Genetic variation and sex differences are missed opportunities for addiction biology.

Concerns about external validity of rodent models and translation of findings across species are often based on narrow investigations of populations with limited diversity. Sources of individual variation - including genetics and sex - are only infrequently encompassed in model organism studies. As with most complex diseases, risk for cocaine use disorder is subject to considerable inter-individual variation. Explicit inclusion of individual differences in rodent research may reveal conserved phenotypes and molecular systems relevant to human addiction. We surveyed cocaine-related traits in both males and females of eight inbred mouse strains whose genomes collectively capture 90% of the genetic diversity of the mouse species. Across these strains, individual differences explained a substantial proportion of variance in cocaine-responsive or cocaine response-predictive behavioral and physiological phenotypes. Wild-derived mouse strains often extended the phenotypic ranges of these behaviors beyond what is observed in conventional laboratory strains. Striatum transcriptional responses to cocaine were also highly dependent upon strain and sex differences; most cocaine-responsive genes were differentially expressed in a manner moderated by strain, sex, or their combination. We compared the strain- and sex-mediated transcriptional responses to cocaine in mice to transcriptomic analysis of people with cocaine use disorder and found that mouse similarity to humans was highly dependent upon mouse genetic background and sex. Specifically, male WSB/EiJ mice and female NOD/ShiLtJ mice exhibited the greatest degree of neural transcriptional consilience with humans with cocaine use disorder. Model organism diversity thus represents a crucial source of biological information that can substantially improve external validity of neuropsychiatric research. Significance StatementLaboratory mice are widely used in research on neurobiological mechanisms of addiction, but most studies use a single strain and often sex of mice. To assess how individual differences in mice modulate addiction-related traits and how this impacts comparative analysis with humans, we studied cocaine-relevant behaviors and brain molecular correlates in both males and females of genetically diverse mouse strains. In this population, individual differences related to sex and/or genetics explain large proportions of differences in cocaine-related traits. Importantly, brain gene expression data demonstrated that some strains mimic human genomic states more readily than others. Individual differences thus represent a crucial and underdeveloped source of biological information about addiction mechanisms that may influence the translational utility of such studies.

neuroscience