Neural Systems, Inhibitory Control, and Methamphetamine Dependence
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PROVIDER: PRJNA340041 | ENA |
REPOSITORIES: ENA
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Project description:<p>The Neural Systems, Inhibitory Control, and Methamphetamine Dependence study started in 2011 and is currently finishing data collection for its last participants. The study included methamphetamine abusing individuals and healthy control participants aged 18-55 years. Participants who qualified over the telephone were scheduled to visit the London Laboratory at the UCLA Semel Institute for Neuroscience and Human Behavior for the In-Person Screening Phase. The screening procedures, usually scheduled over two visits, determined if participants were eligible to complete the subsequent study visits. Both groups completed identical screening procedures, with the exception of more in-depth drug use questions for the methamphetamine users.</p> <p>After providing written consent, participants completed questionnaires about their mood, medical, psychiatric and drug use history, personality and life experiences. They also provided a urine sample to determine what drugs they recently used and a breath sample to determine the carbon monoxide levels in their system. The drug screen tested for recent methamphetamine, cocaine, opiates/opioids, benzodiazepines, THC and other amphetamines. Methamphetamine participants needed to test positive for methamphetamine at admission. If methamphetamine participants tested positive for any drugs other than methamphetamine or marijuana, and if healthy control participants tested positive for any drugs other than marijuana, they were excluded from the study. Additionally, the urine samples of female participants were tested for pregnancy; pregnant females were also excluded. If no exclusionary criteria were met during the first screening visit, participants completed a second screening visit to ensure they were mentally and physically healthy enough to participate. The second screening visit included a psychiatric diagnostic interview (DSM-IV (SCID-I) for first 500 participants and the MINI International Neuropsychiatric Interview M.I.N.I for the last 50 participants). Additionally, laboratory tests and procedures were completed by the UCLA General Clinical Research Center and interpreted by a study physician. Laboratory tests included vital signs (heart rate--BPM, blood pressure, and respirations), an electrocardiogram (ECG) to record the electrical activity of the heart, and an 18-cc blood sample to perform laboratory tests which included a complete chemistry and metabolic panel, hepatic panel, Hepatitis-C tests, and HIV test. The laboratory tests from this blood sample ensured that participants' liver and kidneys were functioning normally, and that their standard blood counts (red cell, white cell, and salts) were also normal. If a Hepatitis-C (HCV) or HIV test was positive, participants were not allowed to continue in the study and their results were reported to the California State Health Department.</p> <p>Participants deemed eligible to continue in the methamphetamine group participated on an outpatient basis or were admitted to the UCLA Medical Center to participate on an inpatient basis for up to 10 days. Typically, detectable levels of methamphetamine in urinalysis remain for 2-3 days, therefore inpatient days 0-3 served as a "washout period" and the methamphetamine abusing inpatient participants provided daily urine samples to test for recent drug use and pregnancy (female participants only). Outpatient participants were also required to remain abstinent from all drugs except nicotine and marijuana for at least 4 days prior to study sessions. Self-reported abstinence for outpatients was verified by urine toxicology and saliva screening at every visit to UCLA before completion of study procedures.</p> <p>Neurocognitive assessments, about three hours each, typically took place on two separate days. The purpose of the neurocognitive sessions were to assess participants' intellectual and neurocognitive functioning. On either the same day as the neurocognitive testing or on separate days, both methamphetamine abusers and healthy controls were administered a structural MRI to collect information on brain structure.</p>
| phs001197 | dbGaP
Project description:Neural Systems, Inhibitory Control, and Methamphetamine Dependence
| PRJNA340042 | ENA
Project description:A genome-wide RNA expression study based on a Phase II randomized placebo-controlled clinical trial of topiramate (TPM) treatment of methamphetamine (METH) dependence. Gene expression data were analyzed based on TPM responses at Weeks 8 and 12, to identify differentially expressed genes and related pathways.
2017-11-17 | GSE107015 | GEO
Project description:Delineating the processes that contribute to the progression and maintenance of substance dependence is critical to understanding and preventing addiction. Several previous studies have shown inhibitory control deficits in individuals with stimulant use disorder. We used a Bayesian computational approach to examine potential neural deficiencies in the dynamic predictive processing underlying inhibitory function among recently abstinent methamphetamine-dependent individuals (MDIs), a population at high risk of relapse. Sixty-two MDIs were recruited from a 28-day inpatient treatment program at the San Diego Veterans Affairs Medical Center and compared with 34 healthy control subjects. They completed a stop-signal task during functional magnetic resonance imaging. A Bayesian ideal observer model was used to predict individuals' trial-to-trial probabilistic expectations of inhibitory response, P(stop), to identify group differences specific to Bayesian expectation and prediction error computation. Relative to control subjects, MDIs were more likely to make stop errors on difficult trials and had attenuated slowing following stop errors. MDIs further exhibited reduced sensitivity as measured by the neural tracking of a Bayesian measure of surprise (unsigned prediction error), which was evident across all trials in the left posterior caudate and orbitofrontal cortex (Brodmann area 11), and selectively on stop error trials in the right thalamus and inferior parietal lobule. MDIs are less sensitive to surprising task events, both across trials and upon making commission errors, which may help explain why these individuals may not engage in switching strategy when the environment changes, leading to adverse consequences.
| S-EPMC5621759 | biostudies-literature
Project description:For human brain microvascular endothelial cells, we used adult passage 3 cortical cells (hBMVECs,
CellSystems, Kirkland, WA, USA). Cells were seeded at 13-15000 cells/cm2 in CSC complete
medium (Cell Systems, Kirkland, WA, USA) on tissue culture plastic culture dishes coated
with Attachment factor for 30 min (Cell Systems, Kirkland, WA, USA).
Methamphetamine (Sigma-Aldrich, St Louis, MO, USA) was
prepared at a stock concentration of 10mM in distilled water. Methamphetamine dilutions 50 micromolar were
made in Endo and Neuro/Astro/Peri media respectively and applied to the cells for 26 hrs.
Further info in
"Proteomic and metabolomic characterization of human neurovascular unit
cells in response to methamphetamine" Herland et al Adv Biosystems 2020
2020-07-20 | MSV000085789 | MassIVE
Project description:Methamphetamine can trigger dopamine releasing in human brain, now used as abuse drug. Some studies have shown that specific genes and proteins responded to, methamphetamine, but little is known about the overall “omic” response of organisms to this illicit substance. Here we demonstrate that Drosophila melanogaster has the potential to give us significant insights into evolutionarily conserved responses to methamphetamine. We performed metabolome, proteome, and transciptome profiling with Drosophila treated with methamphetamine. The proteomic profiling revealed responses associated with known physiological problems that occur with methamphetamine usage in mammals. The metabolomic result showed that the metabolite trehalose was decreased significantly after methamphetamine exposure, suggesting an oxidative stress response to this drug. Many of the differential transcribed genes, including detoxification enzymes, had the potential transcription factor-binding motif YY1 associated with their upstream regulatory regions. YY1 is known to be responsive to amphetamines in mammals.
2010-10-31 | GSE16198 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived hippocampus transcriptome profiling (RNA-seq) in mouse to evaluate alterations in hippocampus with methamphetamine administrations.
2022-01-24 | GSE193829 | GEO
Project description:Methamphetamine can trigger dopamine releasing in human brain, now used as abuse drug. Some studies have shown that specific genes and proteins responded to, methamphetamine, but little is known about the overall omic response of organisms to this illicit substance. Here we demonstrate that Drosophila melanogaster has the potential to give us significant insights into evolutionarily conserved responses to methamphetamine. We performed metabolome, proteome, and transciptome profiling with Drosophila treated with methamphetamine. The proteomic profiling revealed responses associated with known physiological problems that occur with methamphetamine usage in mammals. The metabolomic result showed that the metabolite trehalose was decreased significantly after methamphetamine exposure, suggesting an oxidative stress response to this drug. Many of the differential transcribed genes, including detoxification enzymes, had the potential transcription factor-binding motif YY1 associated with their upstream regulatory regions. YY1 is known to be responsive to amphetamines in mammals. For each sample, 20 virgin male flies were used to extract the mRNA. Three replicates were produced for each treatments. Two treatments were produced (control VS 0.6% 24 h meth-fed).
2010-10-30 | E-GEOD-16198 | biostudies-arrayexpress
Project description:Methamphetamine abuse continues to be a worldwide problem, damaging the individual user as well as society. Only minimal information exists on molecular changes in the brain that result from methamphetamine administered in patterns typical of human abusers. In order to investigate such changes, we examined the effect of methamphetamine on the transcriptional profile in brains of monkeys. Gene expression profiling of the caudate and hippocampus identified protein disulfide isomerase family member A3 (PDIA3) to be significantly up-regulated in the animals treated with methamphetamine as compared to saline treated control monkeys. Treatment of primary rat neurons with methamphetamine revealed an up-regulation of PDIA3, showing a direct effect of methamphetamine on neurons to increase PDIA3. In vitro studies using a neuroblastoma cell line demonstrated that PDIA3 expression protects against methamphetamine-induced cell toxicity and methamphetamine-induced intracellular reactive oxygen species production, revealing a neuroprotective role for PDIA3. The current study implicates PDIA3 to be an important cellular neuroprotective mechanism against a toxic drug, and as a potential target for therapeutic investigations. To study the effects of chronic METH effects on the brain
2011-11-15 | E-GEOD-33707 | biostudies-arrayexpress
Project description:Methamphetamine abuse continues to be a worldwide problem, damaging the individual user as well as society. Only minimal information exists on molecular changes in the brain that result from methamphetamine administered in patterns typical of human abusers. In order to investigate such changes, we examined the effect of methamphetamine on the transcriptional profile in brains of monkeys. Gene expression profiling of the caudate and hippocampus identified protein disulfide isomerase family member A3 (PDIA3) to be significantly up-regulated in the animals treated with methamphetamine as compared to saline treated control monkeys. Treatment of primary rat neurons with methamphetamine revealed an up-regulation of PDIA3, showing a direct effect of methamphetamine on neurons to increase PDIA3. In vitro studies using a neuroblastoma cell line demonstrated that PDIA3 expression protects against methamphetamine-induced cell toxicity and methamphetamine-induced intracellular reactive oxygen species production, revealing a neuroprotective role for PDIA3. The current study implicates PDIA3 to be an important cellular neuroprotective mechanism against a toxic drug, and as a potential target for therapeutic investigations.
2011-11-15 | GSE33707 | GEO