David W. Self

ORCID: 0000-0001-7202-2813
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About
Contact & Profiles
Research Areas
  • Neurotransmitter Receptor Influence on Behavior
  • Receptor Mechanisms and Signaling
  • Neuroscience and Neuropharmacology Research
  • Neuropeptides and Animal Physiology
  • Memory and Neural Mechanisms
  • Neuroendocrine regulation and behavior
  • Nerve injury and regeneration
  • Neurogenesis and neuroplasticity mechanisms
  • Autism Spectrum Disorder Research
  • Stress Responses and Cortisol
  • Nicotinic Acetylcholine Receptors Study
  • Sleep and Wakefulness Research
  • Circadian rhythm and melatonin
  • Gene expression and cancer classification
  • Zebrafish Biomedical Research Applications
  • Adipose Tissue and Metabolism
  • Smoking Behavior and Cessation
  • EEG and Brain-Computer Interfaces
  • Parkinson's Disease Mechanisms and Treatments
  • Pharmacological Receptor Mechanisms and Effects
  • Genetic Mapping and Diversity in Plants and Animals
  • Epigenetics and DNA Methylation
  • Attention Deficit Hyperactivity Disorder
  • Treatment of Major Depression
  • Cannabis and Cannabinoid Research

The University of Texas Southwestern Medical Center
2010-2020

Southwestern Medical Center
2004-2018

Dementia UK
2008

Tufts University
2006

Genomics Institute of the Novartis Research Foundation
2004

Yale University
1994-2003

Connecticut Mental Health Center
1994-1999

Harvard University
1999

University of California, Irvine
1989-1996

The University of Texas Medical Branch at Galveston
1990

Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development this experience-dependent aversion. Gene profiling in nucleus accumbens indicates local obliterates most effects on gene expression within circuit, with...

10.1126/science.1120972 article EN Science 2006-02-09

Recent work implicates regulation of neurogenesis as a form plasticity in the adult rat hippocampus. Given known effects opiates such morphine and heroin on hippocampal function, we examined opiate this brain region. Chronic administration decreased by 42% granule cell layer. A similar effect was seen rats after chronic self-administration heroin. Opiate not mediated changes circulating levels glucocorticoids, because were that received adrenalectomy corticosterone replacement. These...

10.1073/pnas.120552597 article EN Proceedings of the National Academy of Sciences 2000-06-06

Activation of the mesolimbic dopamine system is known to trigger relapse in animal models cocaine-seeking behavior. We found that this “priming” effect was selectively induced by D 2 -like, and not 1 receptor agonists rats. Moreover, -like prevented behavior cocaine itself, whereas enhanced These results demonstrate an important dissociation between - processes support further evaluation as a possible pharmacotherapy for addiction.

10.1126/science.271.5255.1586 article EN Science 1996-03-15

The transcription factor, ΔFosB, is robustly and persistently induced in striatum by several chronic stimuli, such as drugs of abuse, antipsychotic drugs, natural rewards, stress. However, very few studies have examined the degree ΔFosB induction two striatal medium spiny neuron (MSN) subtypes. We make use fluorescent reporter BAC transgenic mice to evaluate dopamine receptor 1 (D1) enriched 2 (D2) MSNs ventral striatum, nucleus accumbens (NAc) shell core, dorsal (dStr) after exposure abuse...

10.1523/jneurosci.1875-13.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-11-20

cAMP-dependent protein kinase (PKA) in the nucleus accumbens (NAc) has been implicated cocaine addiction because (1) reinforcement is mediated by dopamine receptors that modulate cAMP formation, and (2) repeated exposure to upregulates system NAc neurons. This study tested PKA involvement self-administration relapse of cocaine-seeking behavior infusing analogs activate or inhibit into rats. Bilateral intra-NAc infusions inhibitor Rp-cAMPS reduced baseline self-administration, shifted...

10.1523/jneurosci.18-05-01848.1998 article EN cc-by-nc-sa Journal of Neuroscience 1998-03-01

The transcription factor DeltaFosB accumulates in substance P-dynorphin-containing striatal neurons with repeated cocaine use. Here, we show that inducible transgenic overexpression this same cell type facilitates acquisition of self-administration at low-threshold doses, consistent increased sensitivity to the pharmacological effects drug. Importantly, also enhances degree effort mice will exert maintain higher doses on a progressive ratio schedule reinforcement, whereas levels intake are...

10.1523/jneurosci.23-06-02488.2003 article EN Journal of Neuroscience 2003-03-15

The transcription factor DeltaFosB accumulates and persists in brain response to chronic stimulation. This accumulation after exposure drugs of abuse has been demonstrated previously by Western blot most dramatically striatal regions, including dorsal striatum (caudate/putamen) nucleus accumbens. In the present study, we used immunohistochemistry define with greater anatomical precision induction throughout rodent drug treatment. We also extended previous research involving cocaine,...

10.1002/syn.20500 article EN Synapse 2008-02-21

Abstract The transcription factor ΔFosB is induced in the nucleus accumbens and dorsal striatum by chronic exposure to several drugs of abuse, increasing evidence supports possibility that this induction involved addiction process. However, date there has been no report abuse ventral tegmental area (VTA), which also a critical brain reward region. In present study, we used immunohistochemistry demonstrate forced administration cocaine induces rat VTA. This occurs selectively γ‐aminobutyric...

10.1111/j.1460-9568.2005.04110.x article EN European Journal of Neuroscience 2005-05-01

Chronic exposure to addictive drugs enhances cAMP response element binding protein (CREB)-regulated gene expression in nucleus accumbens (NAc), and these effects are thought reduce the positive hedonic of passive cocaine administration. Here, we used viral-mediated transfer produce short- long-term regulation CREB activity NAc shell rats engaging volitional self-administration. Increasing markedly enhanced reinforcement self-administration behavior, as indicated by leftward (long-term)...

10.1523/jneurosci.3070-11.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-11-09

Previous research has shown an increase in tyrosine hydroxylase the ventral tegmental area following chronic morphine and cocaine treatments. Chronic treatment also increases levels of glial fibrillary acidic protein this brain region. In present study, we investigated effects infusing neurotropic factors (nerve growth factor, brain-derived neurotrophic neurotrophin-3, neurotrophin-4 or ciliary factor) via midline intra-ventral cannulae on these biochemical changes. Our studies examined...

10.1016/0306-4522(95)00207-y article EN cc-by-nc-nd Neuroscience 1995-10-01

Previous work has shown that chronic opiate administration regulates protein components of the cAMP signaling pathway, specifically in nucleus accumbens (NAc), a brain region implicated reinforcing properties opiates, and such adaptations may contribute to changes reinforcement mechanisms characterize addiction. In present study, we examined possible role for transcription factor response element-binding (CREB) mediating these long-term effects opiates NAc. Chronic, but not acute, morphine...

10.1016/s0022-3565(25)12267-2 article EN Journal of Pharmacology and Experimental Therapeutics 1996-01-01
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