Selective breeding for oral opioid acceptance or rejection in rats

Carlson, Kristin R.; Saulnier-Dyer, Claudette M.; Moolten, Marjorie S.

doi:10.1016/0091-3057(95)02099-3

Cited by 7 publications

(3 citation statements)

References 41 publications

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“…Selective breeding has been used for generating rodent models with various sensitivities to methamphetamine, opiates, or alcohol or related bio-behavioral traits (Carlson et al 1996; Scibelli et al 2011; Li et al 1993). However, phenotypic selection for differences in nicotine-related physiological changes and behaviors has rarely been done.…”

Section: Discussionmentioning

confidence: 99%

Nine Generations of Selection for High and Low Nicotine Intake in Outbred Sprague–Dawley Rats

Nesil

Kanıt

et al. 2013

Behav Genet

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Previous animal studies have revealed significant involvement of genetics in nicotine intake; however, the extent of the genetic contribution to this behavior has not been well addressed. We report the first study of nine generations of selection for high and low voluntary nicotine intake in outbred Sprague–Dawley rats. Bidirectional mass selection resulted in progressively greater nicotine consumption in the high nicotine-preferring line but no decrease in nicotine intake in the low nicotine-preferring line across generations. Our estimated realized heritability for high voluntary nicotine intake is 0.26 vs close to zero for low voluntary nicotine intake. In contrast, we found no differences between the lines across generations for saccharine intake. These selected lines may provide useful animal models for identifying susceptibility and resistance genes and variants for controlling voluntary nicotine intake in rodents, although we recognize that more generations of selection of these two lines and independent replication of our selection for high and low nicotine-preferring lines are needed.

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Section: Discussionmentioning

confidence: 99%

Nine Generations of Selection for High and Low Nicotine Intake in Outbred Sprague–Dawley Rats

Nesil

Kanıt

et al. 2013

Behav Genet

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“…1991), and motor activity (DeFries & Hegmann 1970), and to many responses to psychoactive drugs (Crabbe et al . 1994; Carlson et al . 1996).…”

Section: Back To the Future: Classical Genetic Methodsmentioning

confidence: 99%

“…Selective breeding has been applied to many complex traits such as active avoidance learning (Brush 1991), aggression (Benus et al 1991), and motor activity (DeFries & Hegmann 1970), and to many responses to psychoactive drugs (Crabbe et al 1994;Carlson et al 1996). A recent selection project shows the utility of selected lines to explore the multiple behavioral assays putatively tapping the same behavioral domain.…”

Section: Selected Linesmentioning

confidence: 99%

Harnessing the mouse to unravel the genetics of human disease

Phillips

Belknap

Hitzemann

et al. 2002

Genes Brain and Behavior

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Complex traits, i.e. those with multiple genetic and environmental determinants, represent the greatest challenge for genetic analysis, largely due to the difficulty of isolating the effects of any one gene amid the noise of other genetic and environmental influences. Methods exist for detecting and mapping the Quantitative Trait Loci (QTLs) that influence complex traits. However, once mapped, gene identification commonly involves reduction of focus to single candidate genes or isolated chromosomal regions. To reach the next level in unraveling the genetics of human disease will require moving beyond the focus on one gene at a time, to explorations of pleiotropism, epistasis and environment-dependency of genetic effects. Genetic interactions and unique environmental features must be as carefully scrutinized as are single gene effects. No one genetic approach is likely to possess all the necessary features for comprehensive analysis of a complex disease. Rather, the entire arsenal of behavioral genomic and other approaches will be needed, such as random mutagenesis, QTL analyses, transgenic and knockout models, viral mediated gene transfer, pharmacological analyses, gene expression assays, antisense approaches and importantly, revitalization of classical genetic methods. In our view, classical breeding designs are currently underutilized, and will shorten the distance to the target of understanding the complex genetic and environmental interactions associated with disease. We assert that unique combinations of classical approaches with current behavioral and molecular genomic approaches will more rapidly advance the field.

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