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David W. Self

Researcher at University of Texas Southwestern Medical Center

Publications -  94
Citations -  15592

David W. Self is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Nucleus accumbens & Dopamine receptor. The author has an hindex of 54, co-authored 94 publications receiving 14649 citations. Previous affiliations of David W. Self include Yale University & University of California, Irvine.

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Essential Role of BDNF in the Mesolimbic Dopamine Pathway in Social Defeat Stress

TL;DR: It is shown that viral-mediated, mesolimbic dopamine pathway–specific knockdown of brain-derived neurotrophic factor is required for the development of experience-dependent social aversion in mice experiencing repeated aggression.
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Molecular Adaptations Underlying Susceptibility and Resistance to Social Defeat in Brain Reward Regions

TL;DR: It is shown that molecular recapitulations of three prototypical adaptations associated with the unsusceptible phenotype are each sufficient to promote resistant behavior and validate a multidisciplinary approach to examine the neurobiological mechanisms of variations in stress resistance.
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Chromatin remodeling is a key mechanism underlying cocaine-induced plasticity in striatum

TL;DR: It is shown that cocaine induces specific histone modifications at different gene promoters in striatum, a major neural substrate for cocaine's behavioral effects, and chromatin remodeling is an important regulatory mechanism underlying cocaine-induced neural and behavioral plasticity.
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Expression of the transcription factor ΔFosB in the brain controls sensitivity to cocaine

TL;DR: It is shown that ΔFosB expression increases the responsiveness of an animal to the rewarding and locomotor-activating effects of cocaine, which supports a model in which Δ FosB, by altering gene expression, enhances sensitivity to cocaine and may thereby contribute to cocaine addiction.
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Opiates inhibit neurogenesis in the adult rat hippocampus.

TL;DR: The findings suggest that opiate regulation of neurogenesis in the adult rat hippocampus may be one mechanism by which drug exposure influences hippocampal function.