共查询到17条相似文献,搜索用时 109 毫秒
1.
成瘾相关记忆的表观遗传学机制 ——药物成瘾研究的新视角 总被引:3,自引:0,他引:3
成瘾相关记忆长期性的脑机制一直是药物成瘾研究领域的难点与热点,该文简要介绍了成瘾记忆长期性分子机制的研究脉络,提示表观遗传学修饰可能是研究药物成瘾的新视角。成瘾药物可以调节染色体不同亚型组蛋白乙酰化水平,不同基因DNA的甲基化程度从而改变染色体的空间结构,进而调节基因的表达导致成瘾,特别是DNA甲基化改变的相对的稳定性可能是成瘾记忆长期存在的分子基础。记忆再巩固过程中学习记忆相关脑区的记忆促进基因与记忆抑制基因的表观遗传学改变可能是未来研究的新趋势 相似文献
2.
3.
4.
反社会行为是受遗传与环境共同影响的不良行为。分子遗传学和神经生物学的研究发现,基因以基因多态性和DNA甲基化的方式影响脑结构、功能及脑内神经递质的产生和释放,进而影响反社会行为的发生发展。本文从基因多态性和DNA甲基化两方面整理了5-HTT、MAOA、OXTR等8个候选基因与反社会行为的关联。并提出未来研究需进一步探讨基因、脑和神经递质对反社会行为的联合作用。同时,扩展多基因位点、基因多态性与DNA甲基化、积极环境与基因交互作用对反社会行为影响的研究,以全面探索反社会行为发生的遗传基础,进而更加有效的预防反社会行为。 相似文献
5.
反社会行为是受遗传与环境共同影响的不良行为。分子遗传学和神经生物学的研究发现,基因以基因多态性和DNA甲基化的方式影响脑结构、功能及脑内神经递质的产生和释放,进而影响反社会行为的发生发展。本文从基因多态性和DNA甲基化两方面整理了5-HTT、MAOA、OXTR等8个候选基因与反社会行为的关联。并提出未来研究需进一步探讨基因、脑和神经递质对反社会行为的联合作用。同时,扩展多基因位点、基因多态性与DNA甲基化、积极环境与基因交互作用对反社会行为影响的研究,以全面探索反社会行为发生的遗传基础,进而更加有效的预防反社会行为。 相似文献
6.
近年来越来越多的研究证据提示, 个体冲动性在成瘾疾患发生发展机制中具有关键作用, 可能成为成瘾行为的潜在易感标记以及早期识别和干预的重要靶点, 但冲动性对不同成瘾行为变化发展的调控机制尚不明确。项目拟综合跨成瘾谱系比较、纵向追踪设计、冲动行为干预等研究途径, 采用人格测量、神经认知、神经影像等技术, 首先比较尼古丁依赖者与网络游戏成瘾者的冲动性结构及其在前额叶–纹状体环路的结构功能改变; 然后采用混合分组设计筛选出具有高低冲动性的非成瘾青少年进行连续追踪研究, 考察冲动性对尼古丁依赖与网络游戏成瘾的预测效力; 并采用认知行为训练, 对吸烟成瘾者与网络游戏成瘾者进行冲动干预, 考察行为干预对冲动性水平及前额叶–纹状体环路功能的改变, 以及对不同成瘾行为发展的抑制后效。旨在探索冲动性作为成瘾的潜在易感标记及干预靶点的效力。 相似文献
7.
药物成瘾是指持续使用成瘾药物, 出现耐受性和戒断症状并严重阻碍正常社会功能的精神疾病。工作记忆在调节药物成瘾行为中扮演了中心角色:在神经易感性和易感人格特质基础上, 低工作记忆容量导致危险决策和去抑制性, 进而影响寻求药物和复吸行为。目前的研究基于已经产生成瘾的个体, 无法区别神经易感性、人格特质以及工作记忆缺陷是药物成瘾的原因还是结果; 而且, 仅从认知角度研究药物成瘾的原因, 会忽视该行为受多个因素影响的事实。 相似文献
8.
9.
介绍了中枢胆碱能系统对吗啡成瘾的影响及其机制。研究结果表明,吗啡成瘾过程中伏隔核等脑区细胞间乙酰胆碱水平发生了改变;去除伏隔核等脑区胆碱能细胞强化了吗啡成瘾行为;胆碱能激动剂和抑制剂都能干预吗啡成瘾、但机制可能不同——前者可能通过与多巴胺能交互作用来实现,后者可能通过干扰记忆或者加速吗啡代谢而发挥作用;胆碱能受体对吗啡成瘾也具有重要影响 相似文献
10.
11.
Decisions about using addictive substances are influenced by distractions by addiction-related stimuli, of which the user might be unaware. The addiction-Stroop task is a paradigm used to assess this distraction. The empirical evidence for the addiction-Stroop effect is critically reviewed, and meta-analyses of alcohol-related and smoking-related studies are presented. Studies finding the strongest effects were those in which participants had strong current concerns about an addictive substance or such concerns were highlighted through experimental manipulations, especially those depriving participants of the substance. Theories to account for addiction-related attentional bias are discussed, of which the motivational theory of current concerns appears to provide the most complete account of the phenomenon. Recommendations are made for maximizing the precision of the addiction-Stroop test in future research. 相似文献
12.
Preliminary evidence suggests that changes in DNA methylation, a widely studied epigenetic mechanism, contribute to the etiology of Autism Spectrum Disorder (ASD). However, data is primarily derived from post-mortem brain samples or peripheral tissue from adults. Deep-phenotyped longitudinal infant cohorts are essential to understand how epigenetic modifications relate to early developmental trajectories and emergence of ASD symptoms. We present a proof-of-principle study designed to evaluate the potential of prospective epigenetic studies of infant siblings of children with ASD.Illumina genome-wide 450 K DNA methylation data from buccal swabs was generated for 63 male infants at multiple time-points from 8 months to 2 years of age (total N = 107 samples). 11 of those infants received a diagnosis of ASD at 3 years. We conducted a series of analyses to characterize DNA methylation signatures associated with categorical outcome and neurocognitive measures from parent-report questionnaire, eye-tracking and electro-encephalography.Effects observed across the entire genome (epigenome-wide association analyses) suggest that collecting DNA methylation samples within infant-sibling designs allows for the detection of meaningful signals with smaller sample sizes than previously estimated. Mapping networks of co-methylated probes associated with neural correlates of social attention implicated enrichment of pathways involved in brain development. Longitudinal modelling found covariation between phenotypic traits and DNA methylation levels in the proximity of genes previously associated with cognitive development, although larger samples and more complete datasets are needed to obtain generalizable results.In conclusion, assessment of DNA methylation profiles at multiple time-points in infant-sibling designs is a promising avenue to comprehend developmental origins and mechanisms of ASD. 相似文献
13.
14.
“遗传与环境”的争论一直是创造力研究的核心问题, 但目前对于环境以及遗传与环境交互作用对创造力影响的分子生物机制还未有研究涉及。近年来, 随着表观遗传学的兴起, 揭示影响心理行为的表观遗传机制现已成为心理学研究的热点。作为环境与基因组之间的纽带, 表观遗传学研究为揭示环境以及遗传与环境交互作用对创造力影响的分子生物机制提供了机遇。本研究以多巴胺相关基因、家庭环境以及两者对于创造力的交互作用为切入点, 对影响创造力的表观遗传机制进行考察, 并在此基础之上, 对环境以及遗传与环境交互作用对创造力影响的分子生物机制进行探索。具体研究内容包括:(1)通过对多巴胺相关基因甲基化模式与创造力关系的系统考察, 筛选出甲基化模式与创造力有关的基因; (2)对筛选出的基因, 进一步考察其甲基化模式在家庭环境及其遗传多态性与家庭环境交互作用对创造力影响中的中介作用。本研究有助于揭示创造力的表观遗传机制, 深化关于遗传与环境对创造力影响的作用机制的理解。 相似文献
15.
为研究慢性温和应激诱导的抑郁大鼠纹状体内前列腺凋亡反应蛋白(prostate apoptosis response-4, par-4)的表达, 及甲基化是否参与par-4基因表达的调控, 将10周龄大鼠随机分为实验组和对照组, 实验组接受慢性温和应激, 对照组不接受实验性处理。于大鼠13周龄时, 采用强迫游泳、糖水偏爱测验测定大鼠的抑郁水平, 以实时定量PCR检测纹状体par-4及多巴胺D2受体(Dopamine receptor D2, DRD2) mRNA表达水平, 免疫印迹法检测纹状体par-4蛋白质表达水平, 用亚硫酸盐测序法检测par-4基因启动子区甲基化水平。结果发现, 与对照组大鼠相比, 实验组大鼠漂浮时间延长, 糖水偏爱率降低, 脑纹状体par-4、DRD2 mRNA及par-4蛋白质表达水平均降低, par-4基因启动子区甲基化水平两组差异不显著。提示慢性温和应激诱导大鼠产生了抑郁样行为, 并能抑制纹状体par-4基因的表达, 而基因甲基化可能并不参与其调控机制。 相似文献
16.
17.
Elisabeth Conradt Brendan Ostlund Dylan Guerin David A. Armstrong Carmen J. Marsit Edward Tronick Lyn LaGasse Barry M. Lester 《Infant mental health journal》2019,40(4):513-522
Caregivers play a critical role in scaffolding infant stress reactivity and regulation, but the mechanisms by which this scaffolding occurs is unclear. Animal models strongly suggest that epigenetic processes, such as DNA methylation, are sensitive to caregiving behaviors and, in turn, offspring stress reactivity. We examined the direct effects of caregiving behaviors on DNA methylation in infants and infant stress reactivity. Infants and mothers (N = 128) were assessed during a free play when infants were 5 months old. Maternal responsiveness and appropriate touch were coded. and infant buccal epithelial cells were sampled to assess for DNA methylation of the glucocorticoid receptor gene, NR3c1 exon 1F. Infant cortisol reactivity was assessed in response to the still-face paradigm. Greater levels of maternal responsiveness and appropriate touch were related to less DNA methylation of specific regions in NR3c1 exon 1F, but only for females. There was no association with maternal responsiveness and appropriate touch or DNA methylation of NR3c1 exon 1F on prestress cortisol or cortisol reactivity. Our results are discussed in relation to programming models that implicate maternal care as an important factor in programing infant stress reactivity. 相似文献