MiRNA expression profiles in the dorsal striatum of a mouse model of nicotine withdrawal
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE280738 | GEO | 2024/10/31
REPOSITORIES: GEO
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Project description:Nicotine dependence is responsible for perpetuating the adverse health effects due to tobacco use, the leading cause of preventable death worldwide. Nicotine is an agonist for nicotinic acetylcholine receptors, which are enriched in the habenulo-interpeduncular withdrawal circuit. Drugs of abuse, including nicotine, induce stable neuroadaptations, requiring protein synthesis through regulation of transcription factors, epigenetic mechanisms, and non-coding RNAs. It also been shown that miRNAs in brain are regulated by nicotine and that miRNA dysregulation contributes to brain dysfunction, including drug addiction. While much is known about the neurocircuitry responsible for the behaviors associated with nicotine reward or withdrawal, the underlying mechanisms of how changes in behavior are induced are less clear. Using miRNA- and mRNA-Seq, we demonstrate that there are widespread changes in both miRNA and mRNA expression in the IPN and MHb during acute nicotine withdrawal. Conserved, differentially expressed miRNAs were predicted to target inversely regulated mRNAs. This dataset represents a valuable resource, identifying a multitude of miRNAs/genes, which upon further study may reveal new mechanisms underlying the neuroadaptations of nicotine dependence and the symptoms of nicotine withdrawal.
2020-01-08 | GSE117069 | GEO
Project description:The mechanism of nicotine dependence and nicotine related pain remains unclear. tRNAs, a major source of small noncoding RNAs (ncRNA), are the immediate areas of research focus, which have an important role in many pathophysiological processes. However, the role of tRNAs on nicotine dependence and related pain hasn’t been explored yet. In this study, our results indicated that the expression profiles of tRNAs have changed in nicotine treated rats as compared with normal rats, and among those, some differentially expressed tRNAs might be novel targets for nicotine dependence or nicotine related pain.
2021-12-31 | GSE162402 | GEO
Project description:DeCODE Genetics of Nicotine Dependence
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Project description:<p>A genome-wide association study on smoking behavior and nicotine dependence in Icelandic smokers, assessed by the number of cigarettes smoked per day, smoking initiation and degree of dependence on nicotine.</p> <p>The number of cigarettes smoked per day was ascertained through questionnaires given to individuals participating in multiple disease projects at deCODE Genetics (n=16,483). Smoking initiation was analyzed by comparing those that have ever smoked (n=16,483) versus those that have never smoked (n=21,667). The nicotine dependence analysis included 3,435 nicotine dependent cases (score 4 or higher on Fagerstrom Test for Nicotine Dependence (FTND) or endorsement of at least three of the seven Diagnostic and Statistical Manual of Mental Disorders 4th edition (DSM-IV) criteria) and 3,344 low-quantity smokers as controls.</p>
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Project description:Sex differences in behaviors relevant to nicotine addiction have been observed in rodent models and human subjects. Behavioral, imaging and epidemiological studies also suggest underlying sex differences in mesolimbic dopamine signaling pathways. In this study we evaluated the proteome in the ventral tegmental area (VTA) and nucleus accumbens (NAc) shell in male and female mice. Experimental groups included two mouse strains (C3H/HeJ and C57BL/6J) at baseline, a sub-chronic, rewarding regimen of nicotine in C3H/HeJ mice, and chronic nicotine administration and withdrawal in C57BL/6J mice. Isobaric labeling with a TMT 10-plex system, sample fractionation, and tandem mass spectrometry were used to quantify changes in protein abundance. Similar or greater numbers of differentially regulated proteins were found between sexes at baseline in C3H/HeJ or C57BL/6J mice than within sexes following their respective regimen of nicotine administration. Despite differences by sex, strain, and nicotine exposure parameters, glial fibrillary acidic protein (GFAP) and dopamine and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32, Ppp1r1b) were repeatedly identified as significantly altered proteins, especially in the VTA. Further, network analyses showed sex- and nicotine-dependent regulation of a number of signaling pathways, including dopaminergic signaling. Sub-chronic nicotine exposure in female mice increased proteins related to dopaminergic signaling in the NAc shell but decreased them in the VTA, whereas the opposite pattern was observed in male mice. In contrast, dopaminergic signaling pathways were similarly upregulated in both male and female VTA after chronic nicotine and withdrawal. Overall, this study identifies significant sex differences in the proteome of the mesolimbic system, at baseline and after nicotine reward or withdrawal, which may help explain differential trajectories and susceptibility to nicotine addiction in males and females.
2021-06-28 | PXD023859 | Pride
Project description:The long-term goal of this project is to establish whether and how chronic nicotine exposure affects nervous system function. The biological targets of nicotine action are diverse members of the superfamily of neurotransmitter-gated ion channels called nicotinic acetylcholine receptors (nAChR). nAChR play multiple, critical roles in chemical signaling throughout the brain and body. They also must be involved in nicotine dependence, which drives tobacco product use responsible for tremendous economic and personal costs. To define changes in gene expression induced by nicotine exposure in a model neuronal cell lines expressing at least two nicotinic receptor subtypes. Nicotine exposure exerst at least some of its effects on nervous system function by altering gene expression. Cells of the SH-SY5Y human neuroblastoma will be exposed to an efficacious dose of nicotine or to control medium for two different periods. Keywords: time-course
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Project description:We used microarrays to determine the effect of prenatal nicotine exposure on gene expression profiles in the striatum of adolescent rats. We found a number of immediate early genes to be differentially expressed due to food-restriction. We compared control (n=8), nicotine exposed (n=7) and a group of animals matched to the food intake of nicotine exposed animals (n=10) to identify gene expression changes associated with prenatal nicotine exposure
2013-09-06 | E-GEOD-50607 | biostudies-arrayexpress
Project description:<p>Nicotine dependence reduces the likelihood of quitting smoking and predicts withdrawal severity, treatment response, and smoking-related health outcomes. Nicotine dependence is a heritable trait (heritability estimates up to 75%), and prior genome-wide association study (GWAS) analyses have firmly established associations with DNA sequence variants in nicotine acetylcholine receptor genes on chromosome 15q25 and at other loci. In this GWAS meta-analysis, 15 independent studies were assembled for a total of 38,602 regular smokers (28,677 Europeans/European Americans and 9,925 African Americans) with nicotine dependence defined by the Fagerström Test for Nicotine Dependence (FTND). FTND scores, which range from 0 (no dependence) to 10 (highest dependence level), were used to categorize nicotine dependence as mild (scores 0-3), moderate (scores 4-6), or severe (scores 7-10). Two of the 15 studies additionally included low-intensity smokers who reported cigarettes per day as <10 but had no data available on the other FTND items and were defined as mildly dependent, given the high concordance rates between these FTND and CPD categories and minimal phenotype misclassification. The cross-ancestry GWAS meta-analysis tested nearly 18 million genotyped and 1000 Genomes-imputed SNPs/indels for association with mild/moderate/severe dependence. The well-known chromosome 15q25 locus was reconfirmed, and a novel chromosome 20q11 locus spanning the DNA (cytosine-5-)-methyltransferase 3 beta (DNMT3B) gene was identified at genome-wide significance. Genome-wide results for the cross-ancestry and ancestry-specific GWAS meta-analyses are provided.</p>
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Project description:The long-term goal of this project is to establish whether and how chronic nicotine exposure affects nervous system function. The biological targets of nicotine action are diverse members of the superfamily of neurotransmitter-gated ion channels called nicotinic acetylcholine receptors (nAChR). nAChR play multiple, critical roles in chemical signaling throughout the brain and body. They also must be involved in nicotine dependence, which drives tobacco product use responsible for tremendous economic and personal costs. To define changes in gene expression induced by nicotine exposure in a model neuronal cell lines expressing at least two nicotinic receptor subtypes. Nicotine exposure exerst at least some of its effects on nervous system function by altering gene expression. Cells of the SH-SY5Y human neuroblastoma will be exposed to an efficacious dose of nicotine or to control medium for two different periods.
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