PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11592851

A murine dopamine neuron-specific cDNA library and microarray: increased COX1 expression during methamphetamine neurotoxicity.

T Barrett·T Xie·Y Piao·O Dillon-Carter·G J Kargul·M K Lim·F J Chrest·R Wersto·D L Rowley·M Juhaszova·L Zhou·M P Vawter·K G Becker·C Cheadle·W H Wood·U D McCann·W J Freed·M S Ko·G A Ricaurte·D M Donovan
View original source ↗Export metadata ↓

Abstract

Due to brain tissue heterogeneity, the molecular genetic profile of any neurotransmitter-specific neuronal subtype is unknown. The purpose of this study was to purify a population of dopamine neurons, construct a cDNA library, and generate an initial gene expression profile and a microarray representative of dopamine neuron transcripts. Ventral mesencephalic dopamine neurons were purified by fluorescent-activated cell sorting from embryonic day 13.5 transgenic mice harboring a 4.5-kb rat tyrosine hydroxylase promoter-lacZ fusion. Nine-hundred sixty dopamine neuron cDNA clones were sequenced and arrayed for use in studies of gene expression changes during methamphetamine neurotoxicity. A neurotoxic dose of methamphetamine produced a greater than twofold up-regulation of the mitochondrial cytochrome c oxidase polypeptide I transcript from adult mouse substantia nigra at 12 h posttreatment. This is the first work to describe a gene expression profile for a neuronal subtype and to identify gene expression changes during methamphetamine neurotoxicity.

Explore related subjects

3,4-Dihydroxyphenylacetic AcidAnimalsDNA, ComplementaryDopamineDopamine Uptake InhibitorsElectron Transport Complex IVEnzyme InductionFemaleGene Expression ProfilingGene LibraryGenes, SyntheticLac OperonMaleMesencephalonMethamphetamineMiceMice, TransgenicMolecular Sequence DataNerve Tissue ProteinsNeuronsOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticRatsTranscription, GeneticTyrosine 3-MonooxygenaseJournal ArticleResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T Barrett, T Xie, Y Piao, O Dillon-Carter, G J Kargul, M K Lim, F J Chrest, R Wersto, D L Rowley, M Juhaszova, L Zhou, M P Vawter, K G Becker, C Cheadle, W H Wood, U D McCann, W J Freed, M S Ko, G A Ricaurte, D M Donovan. 2001. A murine dopamine neuron-specific cDNA library and microarray: increased COX1 expression during methamphetamine neurotoxicity.. https://doi.org/10.1006/nbdi.2001.0423

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Proteasome inhibitor model of Parkinson's disease in mice is confounded by neurotoxicity of the ethanol vehicle.

Defects in the ubiquitin-proteasome system have been implicated in Parkinson's Disease (PD). Recently, a rat model of PD was developed using a synthetic proteasome inhibitor (PSI), (Z-lle-Glu(OtBu)-Ala-Leu-al). We attempted to transfer this model to mouse studies, where genetics can be more readily investigated due to the availability of genetically modified mice. We treated C57BL/6 (B6) mice with six intraperitoneal injections of 6 mg/kg PSI in 50 mul of 70% ethanol over a 2-week-period. We found significant decreases in nigrostriatal dopamine in PSI-treated mice compared with saline-treated mice. However, we observed similar decreases in the ethanol-treated vehicle control group. Administration of ethanol alone led to significant long-term alterations in dopamine levels. Ethanol significantly eclipses the effects of PSI in the dopamine system, and therefore is a confounding vehicle for this model.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2007

Intrastriatal injection of hypoxanthine reduces striatal serotonin content and impairs spatial memory performance in rats.

The aim of this study was to investigate the effects of intrastriatal injection of hypoxanthine, a metabolite accumulated in Lesch-Nyhan disease, on rats' performance in the Morris water maze tasks, along with the monoamine content in striatum of rats. Male adult Wistar rats were divided in two groups: (1) saline-injected and (2) hypoxanthine-injected group. Seven days after solutions infusion, animals were trained in the Morris Water Maze or were sacrificed for evaluation of the striatal monoamine content. Results show that hypoxanthine administration caused impairment on spatial navigation in the acquisition phase in reference memory task in the Morris Water Maze, as well as in the latency to cross over the platform location in probe trial, when compared to the saline group (control). Hypoxanthine also altered rat performance in the working memory. Although striatal dopamine metabolites content did not change, treated animals showed a reduction of tissue levels of serotonin (5-HT) and 5- hydroxyl-indoleacetic acid (5-HIAA). These results show that intra-striatal hypoxanthine administration provoked impairment of spatial learning/memory in rats without affecting striatal dopaminergic system, although serotonergic pathways seem to have been affected.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2007

A history of human-like dieting alters serotonergic control of feeding and neurochemical balance in a rat model of binge-eating.

OBJECTIVE: This study replicated a model of stress-induced binge-eating in rats with a history of caloric restriction (HCR), tested their response to SSRI (fluoxetine) treatment, and explored changes in brain monoamine levels. METHOD: Young female rats with no-HCR/no-Stress, no-HCR/Stress, HCR/no-Stress, and HCR+Stress (binge-eating) were treated with fluoxetine. Post-mortem levels of serotonin, dopamine, and metabolites were assessed from brain regions key to feeding and reward. RESULTS: A 3 mg/kg dose of fluoxetine without effect in the no-HCR groups suppressed intake of HCR groups, normalizing the binge-eating of HCR/Stress rats. No differences in monoamines were detected in the hypothalamus or tegmentum but a strong positive relationship between accumbens serotonin and dopamine turnover in no-HCR rats was absent in rats with HCR. CONCLUSION: Despite lack of hunger, a history of human-like dieting alters serotonin function in ways suggesting consequences not only to feeding but also control of reward and mood that are dependent on dopamine/serotonin interactions.

3,4-Dihydroxyphenylacetic Acid↗