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The Drug Related Gene Database (DRG), funded by National Institute of Drug Abuse (NIDA) ARRA Supplement #HHSN27120080035C, was created to facilitate discovery and use of resources relevant to drug abuse research.  The database and associated tools were specifically created for providing data that is contained in tables, figures and supplementary materials from published papers in a way that facilitates search across the results of these studies.  These data are extracted from published journal articles that directly test hypotheses relevant to the neuroscience of addiction and addictive behavior.  The current database mainly focuses on gene expression data and exposes data from investigations using DNA microarrays, polymerase chain reaction, immunohistochemistry and in-situ hybridizations. Data types include the effects of a particular drug, strain, or knock out on a particular gene, in a particular anatomical region. Once loaded, these data are available for query through the NIF interface.  During this process, the content is standardized using a generic high level description of a relevant study and terms are mapped to ontologies available through the NIF project (NIFSTD) to enhance semantic search of such data. 

Table of Contents:

Publications whose tables are available through DRG

Instructions for authors - submit your data to the DRG

Step by step example of a submission: 

Click here to find step by step instructions using a specific example from Grice et al. (2007) Transcriptional profiling of C57 and DBA strains of mice in the absence and presence of morphine.   BMC Genomics. Mar 16;8:76.  These sample data are included in the Excel template provided in the instructions to authors on the 3rd tab (worksheet) or you may download them directly

Resources for Submission Testers:

Click here for some resources identified for submission testers that may be good to add to the DRG. For your convenience, data has already been extracted.

Database issues below:

Articles requiring a subscription to access:
  • Induction of the drug metabolizing enzyme CYP2D in monkey brain by chronic nicotine treatment.

Table 2. Brain CYP2D protein immunocytochemical staining in saline- and chronic nicotine-treated monkeys

  • Differential modulation of gene expression in the NMDA postsynaptic density of schizophrenic and control smokers.

Table 4. Genes groups differentially expressed between smokers and nonsmokers (P < 0.05)

Table 6. QRT-PCR confirmation of microarray gene expression changes

Supplemental Table 2. Probe sets on the Affymetrix U95Av2 chips for genes expressed in the NMDA postsynaptic density

Supplemental Table 3.  All genes differentially expressed between smokers and nonsmokers (p<0.05)

Supplemental Table 4. All genes differentially expressed by the interaction of schizophrenia x smoking

  • Microarray analysis of genes expressed in the frontal cortex of rats chronically treated with morphine and after naloxone precipitated withdrawal.

Table 2. Results DNA microarrays: chronic morphine treatment vs. saline treatment (control)

Table 3. Results DNA-microarrays: naloxone precipitated morphine withdrawal vs. saline treatment (control)

  • Expression pattern of NuIP gene in adult mouse brain.

Table 1. Summary of brain areas expressing NuIP protein and Nurr1.

  • Zombeck et al., Neuroscience. 2010 Patterns of neural activity associated with differential acute locomotor stimulation to cocaine and methamphetamine in adolescent versus adult male C57BL/6J mice.

Table 1. Mean number of Fos positive cells and associated statistics after saline, 15 or 30 mg/kg cocaine

Table 2. The difference in cocaine-induced Fos between adolescents and adults after correcting for locomotor activity

Table 3. Mean number of Fos positive cells and associated statistics after saline, 2, or 4 mg/kg methamphetamine

Table 4. The difference in methamphetamine-induced Fos between adolescents and adults after correcting for locomotor activity

  • Mitchell et al., Brain Res Dev Brain Res. 2003 c-fos and cleaved caspase-3 expression after perinatal exposure to ethanol, cocaine, or the combination of both drugs.

Fig. 3. Striatal c-fos induction in E22 fetuses: prenatal ethanol and cocaine treatments.

Table 1. Fos expression in neonatal rats at 0, 3, and 24 h after C-section

Table 2. Caspase-3 expression in neonatal rats at 0, 3, and 24 h after C-section

Fig. 6. Striatal caspase-3 induction in E22 fetuses: prenatal ethanol and cocaine treatments.

  • Anghel et al., Neuroscience. 2010 Gene expression profiling following short-term and long-term morphine exposure in mice uncovers genes involved in food intake.

Table 2. Hypothalamic genes with highest fold regulation by morphine

Table 3. Pituitary genes with highest fold regulation by morphine

Table 4. Genes involved in the food intake pathway as elucidated by microarray analysis

Table 5. Real-time RT-PCR results compared with microarray data (expressed as percent of control)

  • Frohmader et al., Neuroscience. 2010 Methamphetamine acts on subpopulations of neurons regulating sexual behavior in male rats.

Table 2. Overview of mating-induced Fos and Meth-induced pERK expression in brain areas where sex and drugs activate non-overlapping neural populations

Table 3. Overview of mating-induced Fos and Meth-induced pERK expression in brain areas where neural activation was induced only by mating

Fig. 2. Sex-induced Fos and Meth-induced pERK expression in Nac, BLA and ACA neurons 10 min following administration of 4mg/kg Meth.

Fig. 4, Sex-induced Fos and Meth-induced pERK expression in NAc, BLA, and ACA neurons 15 min following administration of 4 mg/kg Meth.

  • Novikova et. al., Neurotoxicol Teratol. 2005 Cocaine-induced changes in the expression of apoptosis-related genes in the fetal mouse cerebral wall

Table 1. Apoptosis-related genes affected in the frontal and occipital regions of the fetal mouse cerebral wall by chronic cocaine exposure

Publications without direct link to tables:
  • Differential gene expression in the rat caudate putamen after binge cocaine administration: Advantage of triplicate microarray analysis

                TABLE IV. Partial list of cocaine-regulated genes in the rat caudate putamen

  • Induction of the drug metabolizing enzyme CYP2D in monkey brain by chronic nicotine treatment.

Table 2. Brain CYP2D protein immunocytochemical staining in saline- and chronic nicotine-treated monkeys

  • Transcriptional responses to reinforcing effects of cocaine in the rat hippocampus and cortex.

Table 1: Genes significantly changed after cocaine CPP treatment in the hippocampus

Table 2: Reverse transcriptase--polymerase chain reaction confirmation for selected genes changed after cocaine CPP treatment in the hippocampus and cortex

  • Alcohol-responsive genes in the frontal cortex and nucleus accumbens of human alcoholics.

Table 3 - Differentially expressed genes common to both the NA and PFC.

Table 4 - Comparison of gene expression of selected genes using microarray and RT-PCR.

Table 5 - Differentially expressed genes in the PFC in major functional groups.

Table 6 - Genes differentially expressed in the alcoholic NA in major functional groups.

  • Transcription profiling reveals mitochondrial, ubiquitin and signaling systems abnormalities in postmortem brains from subjects with a history of alcohol abuse or dependence.

Table II. Genes with Altered Expression in Subjects With a History of Alcohol Abuse/Dependence

  • Differential modulation of gene expression in the NMDA postsynaptic density of schizophrenic and control smokers.

Table 4. Genes groups differentially expressed between smokers and nonsmokers (P < 0.05)

Table 6. QRT-PCR confirmation of microarray gene expression changes

Supplemental Table 2. Probe sets on the Affymetrix U95Av2 chips for genes expressed in the NMDA postsynaptic density

Supplemental Table 3.  All genes differentially expressed between smokers and nonsmokers (p<0.05)

Supplemental Table 4. All genes differentially expressed by the interaction of schizophrenia x smoking

  • Gene expression in human alcoholism: microarray analysis of frontal cortex.

Table 2. Myelin-Related Expression Data

Table 3. Genes That Meet the Criteria for Differential Expression on the cDNA (GS-1, GS-2) Array

Table 4. Genes That Meet the Criteria for Differential Expression on the Oligonucleotide (A-1, A-2) Arrays

  • Patterns of gene expression are altered in the frontal and motor cortices of human alcoholics.

Table 4 - Differential expression values for genes involved in global processes

Table 5 - Differential expression values for genes involved in specific signaling processes

  • Gene expression profiling in the striatum of inbred mouse strains with distinct opioid-related phenotypes.

Additional data file 2 - List of probe-sets of genes differentially expressed among the four inbred strains of mice.

Additional data file 3 - Detailed description of Gene Ontology analysis presented in Table 1 and Table 2.

  • Microarray analysis of genes expressed in the frontal cortex of rats chronically treated with morphine and after naloxone precipitated withdrawal.

Table 2. Results DNA microarrays: chronic morphine treatment vs. saline treatment (control)

Table 3. Results DNA-microarrays: naloxone precipitated morphine withdrawal vs. saline treatment (control)

  • Precipitated morphine withdrawal stimulates multiple activator protein-1 signaling pathways in rat brain.

TABLE 1 - Relative lntensity of c-fos mRNA signals in rat brain 1 hr after naloxone-precipitated morphine withdrawal

  • Expression pattern of NuIP gene in adult mouse brain.

Table 1. Summary of brain areas expressing NuIP protein and Nurr1.

  • Edenberg et al., Genes Brain Behav. 2005 Gene expression in the hippocampus of inbred alcohol-preferring and -nonpreferring rats.

Table 3. Genes expressed at significantly (P < /= 0.01) higher levels in hippocampus of iP than iNP rats

Table 4. Genes expressed at significantly (P < /= 0.01) lower levels in the hippocampus of iP than iNP rats

  • Zombeck et al., Neuroscience. 2010 Patterns of neural activity associated with differential acute locomotor stimulation to cocaine and methamphetamine in adolescent versus adult male C57BL/6J mice.

Table 1. Mean number of Fos positive cells and associated statistics after saline, 15 or 30 mg/kg cocaine

Table 2. The difference in cocaine-induced Fos between adolescents and adults after correcting for locomotor activity

Table 3. Mean number of Fos positive cells and associated statistics after saline, 2, or 4 mg/kg methamphetamine

Table 4. The difference in methamphetamine-induced Fos between adolescents and adults after correcting for locomotor activity

  • Mitchell et al., Brain Res Dev Brain Res. 2003 c-fos and cleaved caspase-3 expression after perinatal exposure to ethanol, cocaine, or the combination of both drugs.

Fig. 3. Striatal c-fos induction in E22 fetuses: prenatal ethanol and cocaine treatments.

Table 1. Fos expression in neonatal rats at 0, 3, and 24 h after C-section

Table 2. Caspase-3 expression in neonatal rats at 0, 3, and 24 h after C-section

Fig. 6. Striatal caspase-3 induction in E22 fetuses: prenatal ethanol and cocaine treatments.

  • Anghel et al., Neuroscience. 2010 Gene expression profiling following short-term and long-term morphine exposure in mice uncovers genes involved in food intake.

Table 2. Hypothalamic genes with highest fold regulation by morphine

Table 3. Pituitary genes with highest fold regulation by morphine

Table 4. Genes involved in the food intake pathway as elucidated by microarray analysis

Table 5. Real-time RT-PCR results compared with microarray data (expressed as percent of control)

  • Befort et al., Ann N Y Acad Sci. 2008 Gene expression is altered in the lateral hypothalamus upon activation of the mu opioid receptor.

Table 2. Mu opioid receptor-dependent genes regulated by chronic morphine in the lateral hypothalamus (LH)

Table 3. qPCR analysis of chronic morphine treatments for selected LH genes

  • Frohmader et al., Neuroscience. 2010 Methamphetamine acts on subpopulations of neurons regulating sexual behavior in male rats.

Table 2. Overview of mating-induced Fos and Meth-induced pERK expression in brain areas where sex and drugs activate non-overlapping neural populations

Table 3. Overview of mating-induced Fos and Meth-induced pERK expression in brain areas where neural activation was induced only by mating

Fig. 2. Sex-induced Fos and Meth-induced pERK expression in Nac, BLA and ACA neurons 10 min following administration of 4mg/kg Meth.

Fig. 4, Sex-induced Fos and Meth-induced pERK expression in NAc, BLA, and ACA neurons 15 min following administration of 4 mg/kg Meth.

  • Novikova et. al., Neurotoxicol Teratol. 2005 Cocaine-induced changes in the expression of apoptosis-related genes in the fetal mouse cerebral wall

Table 1. Apoptosis-related genes affected in the frontal and occipital regions of the fetal mouse cerebral wall by chronic cocaine exposure

Publications without direct link to methods (treatment):
  • Regulation of dopaminergic transmission and cocaine reward by the Clock gene
  • Differential gene expression in the rat caudate putamen after binge cocaine administration: Advantage of triplicate microarray analysis
  • Induction of the drug metabolizing enzyme CYP2D in monkey brain by chronic nicotine treatment.
  • Transcriptional responses to reinforcing effects of cocaine in the rat hippocampus and cortex.
  • Transcriptional correlates of human substance use.
  • Alcohol-responsive genes in the frontal cortex and nucleus accumbens of human alcoholics.
  • Transcription profiling reveals mitochondrial, ubiquitin and signaling systems abnormalities in postmortem brains from subjects with a history of alcohol abuse or dependence.
  • Differential modulation of gene expression in the NMDA postsynaptic density of schizophrenic and control smokers.
  • Gene expression in human alcoholism: microarray analysis of frontal cortex.
  • Patterns of gene expression are altered in the frontal and motor cortices of human alcoholics.
  • Gene expression profiling in the striatum of inbred mouse strains with distinct opioid-related phenotypes.
  • Microarray analysis of genes expressed in the frontal cortex of rats chronically treated with morphine and after naloxone precipitated withdrawal.
  • Precipitated morphine withdrawal stimulates multiple activator protein-1 signaling pathways in rat brain.
  • Expression pattern of NuIP gene in adult mouse brain.
  • Edenberg et al., Genes Brain Behav. 2005 Gene expression in the hippocampus of inbred alcohol-preferring and -nonpreferring rats.
  • Zombeck et al., Neuroscience. 2010 Patterns of neural activity associated with differential acute locomotor stimulation to cocaine and methamphetamine in adolescent versus adult male C57BL/6J mice.
  • Mitchell et al., Brain Res Dev Brain Res. 2003 c-fos and cleaved caspase-3 expression after perinatal exposure to ethanol, cocaine, or the combination of both drugs.
  • Anghel et al., Neuroscience. 2010 Gene expression profiling following short-term and long-term morphine exposure in mice uncovers genes involved in food intake.
  • Befort et al., Ann N Y Acad Sci. 2008 Gene expression is altered in the lateral hypothalamus upon activation of the mu opioid receptor.
  • Grice et al., BMC Genomics. 2007 Transcriptional profiling of C57 and DBA strains of mice in the absence and presence of morphine
  • Frohmader et al., Neuroscience. 2010 Methamphetamine acts on subpopulations of neurons regulating sexual behavior in male rats.
  • Novikova et. al., Neurotoxicol Teratol. 2005 Cocaine-induced changes in the expression of apoptosis-related genes in the fetal mouse cerebral wall
Stability of Probe IDs:

Microarray manufacturers were individually questioned about the stability of their probe ids - if they change over time.  For your information, below we have their individual replies:

Illumina:  "The probes ID is an unique internal Illumina reference and can change between chip versions."

and
"Just to clarify, "PROBE_ID" is a unique probe identifier in the Illumina manufacturing database that distinguishes a probe across all products and all species. This should be consistent from chip to chip and if you see the same probe on different versions of a manifest, the probe sequence would be the same."

techsupport@illumina.com

NimbleGen:

"Probe IDs are linked to the design name. If the name is the same, then so are the probe IDs."

and

"The PROBE_IDs within an NDF file are fixed and do not change. So long as the design name (or better yet, the DESIGN_ID) is the same then the PROBE_ID should be stable provided the end user didn't manually edit anything."

"It is worth pointing out that there is no guarantee that PROBE_ID will be unique within a design file. It is always best to HASH on the union of CONTAINER|GENE_EXPR_OPTION, SEQ_ID, and PROBE_ID if you want to insure uniqueness."

biochemts.us@roche.com

Affymetrix:
"The probe ids do not change over time."

"The sequences that they interrogate may change over time because more genes get discovered, and others may change depending on the validation by the scientific community.
The changes for the sequences will be reflected in the annotation updates.
The annotation updates are released three times yearly in mid-March, July and November for all arrays. If there is an update in the genome assembly build for a given organism, that update usually is reflected in the following annotation."

"Annotation updates incorporate current releases from GenBank, RefSeq, Ensembl, UniGene, Entrez Gene, UniProt and UCSC, as well as sequences from other organism-specific databases. The sources for each annotation update since release 20 are documented and available on the NetAffx Support Materials Page."
support@affymetrix.com

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