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Sue Burkhart-Kasch

Researcher at Oregon Health & Science University

Publications -  24
Citations -  2651

Sue Burkhart-Kasch is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Receptor & Sensitization. The author has an hindex of 22, co-authored 24 publications receiving 2550 citations. Previous affiliations of Sue Burkhart-Kasch include Portland VA Medical Center.

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Different data from different labs: lessons from studies of gene-environment interaction.

TL;DR: It is clear that the strong dependence of results on the specific laboratory is itself dependent on the task in question, and laboratory environments probably can never be made sufficiently similar to guarantee identical results on aWide range of tests in a wide range of labs.
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Locomotor Activity in D2 Dopamine Receptor-Deficient Mice Is Determined by Gene Dosage, Genetic Background, and Developmental Adaptations

TL;DR: It is concluded that D2R-deficient mice are not a model of Parkinson’s disease and the interaction of multiple genetic factors in the analysis of complex behaviors in gene knock-out mice is highlighted.
Journal Article

Alcohol preference and sensitivity are markedly reduced in mice lacking dopamine D2 receptors

TL;DR: This paper showed that dopamine signaling via D2 receptors is an essential component of the molecular pathway determining ethanol self-administration and sensitivity, and that D2-receptor-deficient mice showed a marked aversion to ethanol in these mice, relative to the high preference and consumption exhibited by wild-type littermates.
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Alcohol preference and sensitivity are markedly reduced in mice lacking dopamine D2 receptors.

TL;DR: It is demonstrated that dopamine signaling via D 2 receptors is an essential component of the molecular pathway determining ethanol self-administration and sensitivity in D2-receptor-deficient mice.
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Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice.

TL;DR: Results demonstrate locomotor sensitization induced by EtOH, suggest independence of genetic determination of locomotor responses to acute and repeated EtOH exposure, and partially support a relationship between reduced sensitivity to the locomotor stimulant/sensitizing effects of EtOH and EtOH consumption.