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Expression profiles and their potential roles of tRNA-derived small RNAs in hippocampus of nicotine dependence rat

ABSTRACT: Expression profiles and their potential roles of tRNA-derived small RNAs in hippocampus of nicotine dependence rat

PROVIDER: PRJNA681791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13172509.fastq.gz	Fastqsanger.gz
	SRR13172510.fastq.gz	Fastqsanger.gz
	SRR13172511.fastq.gz	Fastqsanger.gz
	SRR13172512.fastq.gz	Fastqsanger.gz
	SRR13172513.fastq.gz	Fastqsanger.gz

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Expression profiles and their potential roles of tRNA-derived small RNAs in hippocampus of nicotine dependence rat

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.

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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:Nicotine intake, whether through tobacco smoking or e-cigarettes, remains a global health concern. An emerging preclinical literature indicates that parental nicotine exposure produces behavioral, physiological, and molecular changes in subsequent generations. However, the heritable effects of voluntary parental nicotine taking are unknown. Here, we show increased acquisition of nicotine taking in male and female offspring of sires that self-administered nicotine. In contrast, self-administration of sucrose and cocaine were unaltered in male and female offspring suggesting that the intergenerational effects of paternal nicotine taking may be reinforcer specific. Further characterization revealed memory deficits and increased anxiety-like behaviors in drug-naïve male, but not female, offspring of nicotine-experienced sires. Using an unbiased, genome-wide approach, we discovered that these phenotypes were associated with decreased expression of Satb2, a transcription factor known to play important roles in synaptic plasticity and memory formation, in the hippocampus of nicotine-sired male offspring. This effect was sex-specific as no changes in Satb2 expression were found in nicotine-sired female offspring. Finally, increasing Satb2 levels in the hippocampus prevented the escalation of nicotine intake and rescued the memory deficits associated with paternal nicotine taking in male offspring. Collectively, these findings indicate that paternal nicotine taking produces heritable sex-specific molecular changes that promote addiction-like phenotypes and memory impairments in male offspring. To characterize the molecular changes associated with the heritable effects of paternal nicotine taking, an unbiased, whole-genome analysis was used to characterize the hippocampal transcriptome of drug-naïve F1 males

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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. Keywords: time-course

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