A5008907230- Neurotransmitter Receptor Influence on Behavior
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Epigenetics and DNA Methylation
- Pancreatic function and diabetes
- Cell death mechanisms and regulation
- Nuclear Receptors and Signaling
- Nerve injury and regeneration
- Genetics and Neurodevelopmental Disorders
- Pain Mechanisms and Treatments
- Neuroendocrine regulation and behavior
- Histone Deacetylase Inhibitors Research
- Adipose Tissue and Metabolism
- Cannabis and Cannabinoid Research
- Autophagy in Disease and Therapy
- Mitochondrial Function and Pathology
- Tryptophan and brain disorders
- Neurogenesis and neuroplasticity mechanisms
- Forensic Toxicology and Drug Analysis
- Cancer-related Molecular Pathways
- Protein Kinase Regulation and GTPase Signaling
- Parkinson's Disease Mechanisms and Treatments
- Pharmacological Receptor Mechanisms and Effects
- Ion channel regulation and function
- Neuroinflammation and Neurodegeneration Mechanisms
National Institute on Drug Abuse
2011-2025
National Institutes of Health
1989-2022
United States Department of Health and Human Services
2009-2022
Parkland Health & Hospital System
2010
Moscow Research and Clinical Center for Neuropsychiatry
2007
Stanley Foundation
1998
National Institute on Aging
1988-1989
Laboratory of Molecular Genetics
1988
Indian Immunologicals (India)
1988
Mayo Clinic
1983
Using cDNA probes to human interleukin 2 (IL2) and receptor (IL2R), the amount of IL2 IL2R mRNA produced by PHA stimulated peripheral blood mononuclear cells from young (less than 40 yr) old (greater 60 donors was quantitated. Stimulated cell cultures each individual were also examined for proliferative ability, expression membrane IL2R, density, shed into culture supernatant. Induction mRNAs decreased in elderly individuals, as levels secretion, percentage IL2R+ T density per cell. The...
Methamphetamine [METH (“speed”)] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs symptoms are thought to be related dysfunctions basal ganglionic structures of the brain. To identify possible molecular bases for these clinical manifestations, we first used cDNA microarray technology measure METH-induced transcriptional responses striatum rats treated with apoptosis-inducing dose drug. METH injection resulted increased...
Methamphetamine (METH) addiction is associated with several neuropsychiatric symptoms. Little known about the effects of METH on gene expression and epigenetic modifications in rat nucleus accumbens (NAC). Our study investigated a non-toxic injection (20 mg/kg) expression, histone acetylation, acetyltransferase (HAT), ATF2, deacetylases (HDACs), HDAC1 HDAC2, that structure. Microarray analyses done at 1, 8, 16 24 hrs after identified METH-induced changes genes previously implicated acute...
Methamphetamine (meth) is an illicit psychostimulant that abused throughout the world. Repeated passive injections of drug given in a single day or over few days cause significant and long-term depletion dopamine serotonin mammalian brain. Because meth self-administration may better mimic some aspects human drug-taking behaviors, we examined to what extent this pattern treatment might also result damage monoaminergic systems Rats were allowed intravenously self-administer (yoked control rats...
Methamphetamine use disorder (MUD) is characterized by loss of control over compulsive drug use. Here, we used a self-administration (SA) model to investigate transcriptional changes associated with the development early and late compulsivity during contingent footshocks. Punishment initially separated methamphetamine taking rats into always shock-resistant (ASR) that continued active lever pressing shock-sensitive (SS) reduced their pressing. At end punishment phase, underwent 15 days...
Bcl-2, an inner mitochondrial membrane protein, inhibits apoptotic neuronal cell death. Expression of Bcl-2 death by decreasing the net cellular generation reactive oxygen species. Studies different investigators have provided unimpeachable evidence a role for oxygen-based free radicals in methamphetamine (METH) -induced neurotoxicity. In addition, studies from our laboratory shown that immortalized rat cells overexpress are protected against METH-induced apoptosis vitro. Moreover,...
Epigenetic consequences of exposure to psychostimulants are substantial but the relationship these changes compulsive drug taking and abstinence is not clear. Here, we used a paradigm that helped segregate rats reduce or stop their methamphetamine (METH) intake (nonaddicted) from those continue take compulsively (addicted) in presence footshocks. We model investigate potential alterations global DNA hydroxymethylation nucleus accumbens (NAc) because neuroplastic NAc may participate...
Methamphetamine (METH) is a neurodegenerative drug of abuse. Its toxicity characterized by destruction monoaminergic terminals and apoptosis in cortical striatal cell bodies. Multiple factors appear to control METH neurotoxicity, including free radicals transcription factors. Here, using cDNA arrays, we show the temporal profile gene expression patterns cortex mice treated with this drug. We obtained two changes from 588 genes surveyed. First, an early pattern upregulation factors, members...
Methamphetamine (METH) is an illicit toxic psychostimulant which widely abused. Its effects depend on the release of excessive levels dopamine (DA) that activates striatal DA receptors. Inhibition DA-mediated neurotransmission by D1 receptor antagonist, SCH23390, protects against METH-induced neuronal apoptosis. The initial purpose present study was to investigate, using microarray analyses, influence SCH23390 transcriptional responses in rat striatum caused a single METH injection at 2 and...
Methamphetamine (METH) addiction is a biopsychosocial disorder that accompanied by multiple relapses even after prolonged abstinence, suggesting the possibilities of long-lasting maladaptive epigenetic changes in brain. Here, we show METH administration produced time-dependent increases expression corticotropin-releasing hormone (Crh/Crf), arginine vasopressin (Avp), and cocaine- amphetamine-regulated transcript prepropeptide (Cartpt) mRNAs rat nucleus accumbens (NAc). Chromatin...
Repeated exposure to the opioid agonist, oxycodone, can lead addiction. Here, we sought identify potential neurobiological consequences of withdrawal from escalated and non-escalated oxycodone self-administration in rats. To reach these goals, used short-access (ShA) (3 h) long-access (LgA) (9 followed by protracted forced abstinence. After 31 days withdrawal, quantified mRNA protein levels receptors rat dorsal striatum hippocampus. Rats LgA, but not ShA, group exhibited escalation SA, with...
Methamphetamine (METH) use disorder is prevalent worldwide. There are reports of sex differences in quantities drug used and relapses to among individuals with METH disorder. However, the molecular neurobiology these potential remains unknown.We trained rats self-administer (0. 1 mg/kg/infusion, i.v.) on an fixed-ratio-1 schedule for 20 days using two 3-hour daily sessions separated by 30-minute breaks. At end self-administration training, underwent tests cue-induced seeking withdrawal 3 30....
Methamphetamine (METH) is an illicit drug which neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels brains of animals exposed moderate-to-large METH doses given within short intervals time. In contrast, repeated injections small nontoxic followed by a challenge with toxic afford protection against monoamine depletion. The present study was undertaken test possibility that might be accompanied transcriptional changes...
METH is an illicit drug of abuse that influences gene expression in the rat striatum. Histone modifications regulate transcription. We therefore used microarray analysis and genome-scale approaches to examine potential relationships between effects on DNA binding histone H4 acetylated at lysine 4 (H4K5Ac) dorsal striatum METH-naïve METH-pretreated rats. Acute chronic administration caused differential changes striatal expression. also increased H4K5Ac around transcriptional start sites...