Neurobiology of Stress最新文献

英文中文

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

Shared genetic risk and causal associations between Post-traumatic stress disorder and migraine with antithrombotic agents and other medications 抗血栓药物和其他药物在创伤后应激障碍和偏头痛之间的共同遗传风险和因果关系。

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01 DOI: 10.1016/j.ynstr.2024.100703

Charlotte K. Bainomugisa , The International Headache Genetics Consortium (IHGC), Dagmar Bruenig , Heidi G. Sutherland , Lyn R. Griffiths , Dale R. Nyholt , Divya Mehta

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that frequently co-occurs with pain disorders including migraine. There are proposed biological, genetic and environmental factors associated with both PTSD and migraine suggesting shared etiology. Genome-Wide Association Studies (GWAS) have been used to identify genomic risk loci associated with various disorders and to investigate genetic overlap between traits. There is a significant genetic correlation between PTSD and migraine with no evidence of a causal relationship that could be attributed to pleiotropy. Cross-disorder genetic analyses were applied to investigate the genetic overlap and causal associations using GWAS summary statistics of PTSD (n = 214408), migraine (n = 873341) and 23 medication use traits (n = 78808–305913) including anti-depressants, anti-migraine preparations and beta-blocking agents.

Across the entire genome, anti-thrombotic agents had a significant and negative genetic correlation with PTSD (rG = −0.2, P_FDR = 0.032) and a positive genetic correlation with migraine (rG = 0.26, P_FDR = 2.23 x 10⁻⁸). PTSD showed significant genetic correlation with 11 other medication use traits including beta blocking agents (rG = −0.11, P_FDR = 0.034). Of the 2495 genomic regions tested, PTSD showed significant local genetic correlation with 12 medication use traits at 43 loci; while migraine showed significant genetic correlation with only anti-inflammatory agents and anti-rheumatic products at locus 12:57522282–57607142 (DAB1) (P < 2 x 10⁻⁵). The genetic liability to PTSD had a causal effect on increased risk of using pain medication such as opioids (β_ivw = 0.59, P = 5.21 x 10⁻⁵) while the genetic liability to migraine had a causal effect on the increased risk of using anti-thrombotic agents (β_ivw = 0.59, P = 1.69 x 10⁻⁷). The genes in the genomic regions shared between PTSD and medication use traits were enriched in neural-related pathways such as neuron development, neurogenesis and protein kinase activity. These results provide further insight into the genetically controlled biological and environmental factors underlying the shared etiology between PTSD and migraine. The identified biomarkers can be used as a basis for investigation as potential drug targets for both disorders. These findings are significant for drug re-purposing and treatment of PTSD and migraine using monotherapy.

创伤后应激障碍（PTSD）是一种精神障碍，经常与偏头痛等疼痛障碍共同发生。目前提出的生物、遗传和环境因素与创伤后应激障碍和偏头痛有关，这表明它们有共同的病因。全基因组关联研究（GWAS）已被用于识别与各种疾病相关的基因组风险位点，并研究性状之间的遗传重叠。创伤后应激障碍和偏头痛之间存在显著的遗传相关性，但没有证据表明其与多效性之间存在因果关系。交叉障碍遗传分析应用GWAS汇总统计研究PTSD （n = 214408）、偏头痛（n = 873341）和23种药物使用特征（n = 78808-305913）（包括抗抑郁药、抗偏头痛制剂和β -阻滞剂）的遗传重叠和因果关系。在整个基因组中，抗血栓药物与PTSD具有显著的负遗传相关性（rG = -0.2, P FDR = 0.032），与偏头痛具有正遗传相关性（rG = 0.26, P FDR = 2.23 × 10-8）。PTSD与包括阻断剂在内的其他11种药物使用特征具有显著的遗传相关性（rG = -0.11, P FDR = 0.034）。在测试的2495个基因组区域中，PTSD与43个位点的12个药物使用特征显示出显著的局部遗传相关性；而偏头痛仅与抗炎药和抗风湿药物在基因座12:57522282-57607142 (DAB1) （P -5）有显著的遗传相关性。PTSD遗传倾向与阿片类药物使用风险增加有因果关系（β ivw = 0.59, P = 5.21 x 10-5），偏头痛遗传倾向与抗血栓药物使用风险增加有因果关系（β ivw = 0.59, P = 1.69 x 10-7）。在创伤后应激障碍和药物使用特征之间共享的基因组区域中，基因在神经元发育、神经发生和蛋白激酶活性等神经相关途径中富集。这些结果为PTSD和偏头痛之间共同病因的遗传控制的生物和环境因素提供了进一步的见解。鉴定的生物标志物可作为研究这两种疾病的潜在药物靶点的基础。这些发现对药物再利用和使用单一疗法治疗PTSD和偏头痛具有重要意义。

{"title":"Shared genetic risk and causal associations between Post-traumatic stress disorder and migraine with antithrombotic agents and other medications","authors":"Charlotte K. Bainomugisa , The International Headache Genetics Consortium (IHGC), Dagmar Bruenig , Heidi G. Sutherland , Lyn R. Griffiths , Dale R. Nyholt , Divya Mehta","doi":"10.1016/j.ynstr.2024.100703","DOIUrl":"10.1016/j.ynstr.2024.100703","url":null,"abstract":"<div><div>Post-traumatic stress disorder (PTSD) is a psychiatric disorder that frequently co-occurs with pain disorders including migraine. There are proposed biological, genetic and environmental factors associated with both PTSD and migraine suggesting shared etiology. Genome-Wide Association Studies (GWAS) have been used to identify genomic risk loci associated with various disorders and to investigate genetic overlap between traits. There is a significant genetic correlation between PTSD and migraine with no evidence of a causal relationship that could be attributed to pleiotropy. Cross-disorder genetic analyses were applied to investigate the genetic overlap and causal associations using GWAS summary statistics of PTSD (<em>n</em> = 214408), migraine (<em>n</em> = 873341) and 23 medication use traits (<em>n</em> = 78808–305913) including anti-depressants, anti-migraine preparations and beta-blocking agents.</div><div>Across the entire genome, anti-thrombotic agents had a significant and negative genetic correlation with PTSD (rG = −0.2, <em>P</em><sub>FDR</sub> = 0.032) and a positive genetic correlation with migraine (rG = 0.26, <em>P</em><sub>FDR</sub> = 2.23 x 10<sup>−8</sup>). PTSD showed significant genetic correlation with 11 other medication use traits including beta blocking agents (rG = −0.11, <em>P</em><sub>FDR</sub> = 0.034). Of the 2495 genomic regions tested, PTSD showed significant local genetic correlation with 12 medication use traits at 43 loci; while migraine showed significant genetic correlation with only anti-inflammatory agents and anti-rheumatic products at locus 12:57522282–57607142 (<em>DAB1</em>) (<em>P</em> < 2 x 10<sup>−5</sup>). The genetic liability to PTSD had a causal effect on increased risk of using pain medication such as opioids (<em>β</em><sub>ivw</sub> = 0.59, <em>P</em> = 5.21 x 10<sup>−5</sup>) while the genetic liability to migraine had a causal effect on the increased risk of using anti-thrombotic agents (<em>β</em><sub>ivw</sub> = 0.59, <em>P</em> = 1.69 x 10<sup>−7</sup>). The genes in the genomic regions shared between PTSD and medication use traits were enriched in neural-related pathways such as neuron development, neurogenesis and protein kinase activity. These results provide further insight into the genetically controlled biological and environmental factors underlying the shared etiology between PTSD and migraine. The identified biomarkers can be used as a basis for investigation as potential drug targets for both disorders. These findings are significant for drug re-purposing and treatment of PTSD and migraine using monotherapy.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"34 ","pages":"Article 100703"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Social context modulates active avoidance: Contributions of the anterior cingulate cortex in male and female rats 社会环境调节主动回避：雄性和雌性大鼠前扣带皮层的贡献。

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01 DOI: 10.1016/j.ynstr.2024.100702

Shannon Ruble, Karissa Payne, Cassandra Kramer, Lexe West, Halle Ness, Greg Erickson, Alyssa Scott, Maria M. Diehl

Actively avoiding danger is necessary for survival. Most research on active avoidance has focused on the behavioral and neurobiological processes when individuals learn to avoid alone, within a solitary context. Therefore, little is known about how social context affects active avoidance. Using a modified version of the platform-mediated avoidance task in rats, we investigated whether the presence of a social partner attenuates conditioned freezing and enhances avoidance compared to avoidance in a solitary context. Rats spent a similar amount of time avoiding during either context; however, rats trained in the social context exhibited greater freezing as well as lower rates of darting and food seeking compared to rats trained in the solitary context. In addition, we observed higher levels of avoidance in females compared to males in the solitary context, but this sex difference was not present in rats trained in the social context. To gain greater mechanistic insight, we optogenetically inactivated glutamatergic projection neurons in the anterior cingulate cortex (ACC) following avoidance training in either context. After avoidance was learned in a social context, photoinactivation of ACC reduced expression of avoidance during a test when the social partner was absent, but not when the partner was present. Our findings suggest a novel contribution of the ACC in avoidance that is learned with a social partner, which has translational implications for understanding ACC dysfunction in those suffering from trauma-related disorders.

积极躲避危险是生存的必要条件。大多数关于主动回避的研究都集中在行为和神经生物学过程上，当个体在一个单独的环境中学会独自回避时。因此，人们对社会环境如何影响主动回避知之甚少。使用平台介导的大鼠回避任务的改进版本，我们研究了与单独情境下的回避相比，社会伴侣的存在是否会减弱条件冻结并增强回避。在两种情况下，大鼠都花了相似的时间来躲避；然而，与在单独环境中训练的老鼠相比，在社会环境中训练的老鼠表现出更大的冻结，以及更低的飞奔和寻找食物的比率。此外，我们观察到，在独处环境中，雌性老鼠的回避程度比雄性老鼠高，但在社交环境中，这种性别差异并不存在。为了获得更深入的机制，我们在两种情况下的回避训练后，通过光遗传学灭活了前扣带皮层（ACC）中的谷氨酸能投射神经元。在社交环境中学会回避后，当社交伴侣不在场时，ACC的光失活会减少回避的表达，但当社交伴侣在场时则不会。我们的研究结果表明，前扣带皮层在逃避行为中的新贡献是与社会伙伴一起学习的，这对理解创伤相关疾病患者的前扣带皮层功能障碍具有转化意义。

{"title":"Social context modulates active avoidance: Contributions of the anterior cingulate cortex in male and female rats","authors":"Shannon Ruble, Karissa Payne, Cassandra Kramer, Lexe West, Halle Ness, Greg Erickson, Alyssa Scott, Maria M. Diehl","doi":"10.1016/j.ynstr.2024.100702","DOIUrl":"10.1016/j.ynstr.2024.100702","url":null,"abstract":"<div><div>Actively avoiding danger is necessary for survival. Most research on active avoidance has focused on the behavioral and neurobiological processes when individuals learn to avoid alone, within a solitary context. Therefore, little is known about how social context affects active avoidance. Using a modified version of the platform-mediated avoidance task in rats, we investigated whether the presence of a social partner attenuates conditioned freezing and enhances avoidance compared to avoidance in a solitary context. Rats spent a similar amount of time avoiding during either context; however, rats trained in the social context exhibited greater freezing as well as lower rates of darting and food seeking compared to rats trained in the solitary context. In addition, we observed higher levels of avoidance in females compared to males in the solitary context, but this sex difference was not present in rats trained in the social context. To gain greater mechanistic insight, we optogenetically inactivated glutamatergic projection neurons in the anterior cingulate cortex (ACC) following avoidance training in either context. After avoidance was learned in a social context, photoinactivation of ACC reduced expression of avoidance during a test when the social partner was absent, but not when the partner was present. Our findings suggest a novel contribution of the ACC in avoidance that is learned with a social partner, which has translational implications for understanding ACC dysfunction in those suffering from trauma-related disorders.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"34 ","pages":"Article 100702"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

引用次数: 0

首页上一页

下一页尾页

类型

全部化学•材料生命科学医学物理工程技术环境•农林材料科学地球科学法学管理学化学环境科学与生态学计算机科学教育学经济学农林科学人文科学生物学数学物理与天体物理心理学综合性期刊其他工业工程理学历史学农学文学信息工程

数据库

全部 ACS Publications Elsevier ieeexplore Springer The Royal Society of Chemistry Wiley

期刊

Neurobiology of Stress

全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.

﹀