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Brain correlates and functional connectivity linking stress, autonomic dysregulation, and alcohol motivation 与压力、自律神经失调和酗酒动机有关的大脑相关性和功能连通性
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-21 DOI: 10.1016/j.ynstr.2024.100645
Dongju Seo , Jorge S. Martins , Rajita Sinha

High stress is a key risk factor for alcohol use disorder (AUD) and often accompanied by physiological dysregulation including autonomic nervous system (ANS) disruptions. However, neural mechanisms underlying drinking behaviors associated with stress and ANS disruptions remain unclear. The current study aims to understand neural correlates of stress, ANS disruptions, and subsequent alcohol intake in social drinkers with risky drinking. Using functional magnetic resonance imaging (fMRI), we investigated brain and heart rate (HR) autonomic responses during brief exposure to stress, alcohol, and neutral cues utilizing a well-validated, individualized imagery paradigm in 48 social drinkers of which 26 reported high-risk drinking (HD) while 22 reported low-risk drinking (LD) patterns. Results indicated that HD individuals showed stress and ANS disruptions with increased basal HR, stress-induced craving, and decreased brain response to stress exposure in frontal-striatal regions including the ventromedial prefrontal cortex (VmPFC), anterior cingulate cortex, striatum, insula, and temporal gyrus. Furthermore, whole-brain correlation analysis indicated that greater basal HR was associated with hypoactive VmPFC, but hyperactive medulla oblongata (MOb) responses during stress, with an inverse association between activity in the VmPFC and Mob (whole-brain corrected (WBC), p < 0.05). Functional connectivity with the MOb as a seed to the whole brain indicated that HD versus LD had decreased functional connectivity between the VmPFC and MOb during stress (WBC, p < 0.05). In addition, those with more compromised functional connectivity between the VmPFC and MOb during stress consumed greater amount of alcohol beverage during an experimental alcohol taste test conducted on a separate day, as well as in their self-reported weekly alcohol intake. Together, these results indicate that stress-related, dysfunctional VmPFC control over brain regions of autonomic arousal contributes to greater alcohol motivation and may be a significant risk factor for hazardous alcohol use in non-dependent social drinkers. Findings also suggest that restoring VmPFC integrity in modulating autonomic arousal during stress may be critical for preventing the development of AUD.

高度压力是导致酒精使用障碍(AUD)的一个关键风险因素,通常伴随着生理失调,包括自律神经系统(ANS)紊乱。然而,与压力和自律神经系统紊乱相关的饮酒行为的神经机制仍不清楚。本研究旨在了解有饮酒风险的社交饮酒者的压力、自律神经系统紊乱和随后酒精摄入的神经相关性。我们采用功能磁共振成像(fMRI)技术,利用一种经过充分验证的个性化想象范式,对 48 名社交饮酒者(其中 26 人报告了高风险饮酒(HD),22 人报告了低风险饮酒(LD)模式)在短暂暴露于压力、酒精和中性线索时的大脑和心率(HR)自律神经反应进行了调查。结果表明,高危饮酒者表现出压力和自律神经系统紊乱,基础心率升高,压力诱发渴求,大脑对压力暴露的额叶-前额叶区域反应减弱,包括腹外侧前额叶皮层(VmPFC)、前扣带回皮层、纹状体、岛叶和颞回。此外,全脑相关性分析表明,在应激时,基础心率越大,VmPFC的反应越不活跃,而延髓(MOb)的反应却越活跃,VmPFC的活动与Mob之间存在反向关联(全脑校正(WBC),p <0.05)。以MOb作为全脑种子的功能连通性表明,在应激期间,HD与LD相比,VmPFC与MOb之间的功能连通性降低(WBC,p <0.05)。此外,应激时VmPFC和MOb之间的功能连通性受损更严重的人在单独一天进行的实验性酒精味觉测试中摄入了更多的酒精饮料,他们自我报告的每周酒精摄入量也更高。这些结果表明,与压力相关的、对自律神经唤醒脑区功能失调的VmPFC控制导致了更大的饮酒动机,并可能成为非依赖性社交饮酒者危险饮酒的一个重要风险因素。研究结果还表明,恢复 VmPFC 在应激时调节自律神经唤醒的完整性可能对预防 AUD 的发生至关重要。
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引用次数: 0
Omega-3 alleviates behavioral and molecular changes in a mouse model of stress-induced juvenile depression 欧米伽-3 可缓解压力诱发的青少年抑郁症小鼠模型的行为和分子变化
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-20 DOI: 10.1016/j.ynstr.2024.100646
Tatyana Strekalova , Daniel Radford-Smith , Isobel K. Dunstan , Anna Gorlova , Evgeniy Svirin , Elisaveta Sheveleva , Alisa Burova , Sergey Morozov , Aleksey Lyundup , Gregor Berger , Daniel C. Anthony , Susanne Walitza

Introduction

Depression is increasingly diagnosed in adolescence, necessitating specific prevention and treatment methods. However, there is a lack of animal models mimicking juvenile depression. This study explores a novel model using ultrasound (US) stress in juvenile mice.

Methods

We employed the US stress model in one-month-old C57/BL6 mice, exposing them to alternating ultrasound frequencies (20–25 kHz and 25–45 kHz) for three weeks. These frequencies correspond to negative and neutral emotional states in rodents and can induce a depressive-like syndrome. Concurrently, mice received either an omega-3 food supplement (FS) containing eicosapentaenoic acid (EPA; 0.55 mg/kg/day) and docosahexaenoic acid (DHA; 0.55 mg/kg/day) or a vehicle. Post-stress, we evaluated anxiety- and depressive-like behaviors, blood corticosterone levels, brain expression of pro-inflammatory cytokines, and conducted metabolome analysis of brain, liver and blood plasma.

Results

US-exposed mice treated with vehicle exhibited decreased sucrose preference, a sign of anhedonia, a key feature of depression, increased anxiety-like behavior, elevated corticosterone levels, and enhanced TNF and IL-1β gene expression in the brain. In contrast, US-FS mice did not display these changes. Omega-3 supplementation also reduced anxiety-like behavior in non-stressed mice. Metabolomic analysis revealed US-induced changes in brain energy metabolism, with FS increasing brain sphingomyelin. Liver metabolism was affected by both US and FS, while plasma metabolome changes were exclusive to FS. Brain glucose levels correlated positively with activity in anxiety tests.

Conclusion

Chronic omega-3 intake counteracted depressive- and anxiety-like behaviors in a US model of juvenile depression in mice. These effects likely stem from the anti-inflammatory properties of the supplement, suggesting potential therapeutic applications in juvenile depression.

导言:越来越多的青少年被诊断出患有抑郁症,因此需要采取特殊的预防和治疗方法。然而,目前还缺乏模拟青少年抑郁症的动物模型。本研究利用超声波(US)应激在幼年小鼠中探索了一种新的模型。方法我们在一个月大的C57/BL6小鼠中采用了US应激模型,将它们暴露于交替的超声波频率(20-25 kHz和25-45 kHz)中,持续三周。这些频率与啮齿动物的负面和中性情绪状态相对应,可诱发类似抑郁症的综合征。与此同时,小鼠接受含有二十碳五烯酸(EPA;0.55 毫克/千克/天)和二十二碳六烯酸(DHA;0.55 毫克/千克/天)的欧米加-3 食物补充剂(FS)或药物。应激后,我们评估了小鼠的焦虑和抑郁样行为、血液中皮质酮的水平、大脑中促炎细胞因子的表达,并对大脑、肝脏和血浆进行了代谢组分析。相比之下,US-FS 小鼠没有出现这些变化。补充 Omega-3 还能减少非应激小鼠的焦虑样行为。代谢组分析显示,US诱导了大脑能量代谢的变化,FS增加了大脑鞘磷脂。肝脏代谢同时受到 US 和 FS 的影响,而血浆代谢组的变化则是 FS 独有的。脑葡萄糖水平与焦虑测试中的活动呈正相关。这些效果可能源于补充剂的抗炎特性,表明它在青少年抑郁症方面具有潜在的治疗用途。
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引用次数: 0
The role of resilience in the relationship between stress and alcohol 复原力在压力与酒精关系中的作用
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-16 DOI: 10.1016/j.ynstr.2024.100644
Melanie L. Schwandt , Eva Cullins , Vijay A. Ramchandani

Stress plays a well-documented role in alcohol consumption and the risk for developing alcohol use disorder. The concept of resilience - coping with and successfully adapting to stressful life experiences – has received increasing attention in the field of addiction research in recent decades, and there has been an accumulation of evidence for resilience as a protective factor against problematic alcohol consumption, risk for alcohol use disorder, disorder severity, and relapse. The conceptual and methodological approaches used in the generation of this evidence vary considerably across investigations, however. In light of this, we carried out this review in order to provide a more thorough understanding of the meaning and scope of resilience, what factors contribute to resilience, how it is measured, and how it relates to alcohol-associated phenotypes. Implications for treatment through the use of resilience-building interventions are likewise discussed, as well as implications for future research on the role of resilience in the etiology and clinical outcomes of alcohol use disorder.

压力在酒精消费和酒精使用障碍的发病风险中扮演着有据可查的角色。近几十年来,抗压能力的概念--应对并成功适应生活中的压力经历--在成瘾研究领域受到越来越多的关注,已有越来越多的证据表明,抗压能力是防止问题酒精消费、酒精使用障碍风险、障碍严重程度和复发的保护因素。然而,不同的研究在得出这些证据时所使用的概念和方法却大相径庭。有鉴于此,我们撰写了这篇综述,以便更透彻地了解复原力的含义和范围、哪些因素有助于提高复原力、如何衡量复原力以及复原力与酒精相关表型之间的关系。此外,还讨论了通过使用抗逆力建设干预措施进行治疗的意义,以及未来研究抗逆力在酒精使用障碍的病因学和临床结果中的作用的意义。
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引用次数: 0
Coffee polyphenols ameliorate early-life stress-induced cognitive deficits in male mice 咖啡多酚可改善雄性小鼠早期生活压力引起的认知缺陷
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-15 DOI: 10.1016/j.ynstr.2024.100641
J. Geertsema , M. Kratochvil , R. González-Domínguez , S. Lefèvre-Arbogast , D.Y. Low , A. Du Preez , H. Lee , M. Urpi-Sarda , A. Sánchez-Pla , L. Aigner , C. Samieri , C. Andres-Lacueva , C. Manach , S. Thuret , P.J. Lucassen , A. Korosi

Stress exposure during the sensitive period of early development has been shown to program the brain and increases the risk to develop cognitive deficits later in life. We have shown earlier that early-life stress (ES) leads to cognitive decline at an adult age, associated with changes in adult hippocampal neurogenesis and neuroinflammation. In particular, ES has been shown to affect neurogenesis rate and the survival of newborn cells later in life as well as microglia, modulating their response to immune or metabolic challenges later in life. Both of these processes possibly contribute to the ES-induced cognitive deficits. Emerging evidence by us and others indicates that early nutritional interventions can protect against these ES-induced effects through nutritional programming. Based on human metabolomics studies, we identified various coffee-related metabolites to be part of a protective molecular signature against cognitive decline in humans. Caffeic and chlorogenic acids are coffee-polyphenols and have been described to have potent anti-oxidant and anti-inflammatory actions. Therefore, we here aimed to test whether supplementing caffeic and chlorogenic acids to the early diet could also protect against ES-induced cognitive deficits. We induced ES via the limited nesting and bedding paradigm in mice from postnatal(P) day 2–9. On P2, mice received a diet to which 0.02% chlorogenic acid (5-O-caffeoylquinic acid) + 0.02% caffeic acid (3′,4′-dihydroxycinnamic acid) were added, or a control diet up until P42. At 4 months of age, all mice were subjected to a behavioral test battery and their brains were stained for markers for microglia and neurogenesis. We found that coffee polyphenols supplemented early in life protected against ES-induced cognitive deficits, potentially this is mediated by the survival of neurons or microglia, but possibly other mechanisms not studied here are mediating the effects. This study provides additional support for the potential of early nutritional interventions and highlights polyphenols as nutrients that can protect against cognitive decline, in particular for vulnerable populations exposed to ES.

事实证明,在早期发育的敏感时期受到的压力会对大脑产生影响,并增加日后出现认知障碍的风险。我们早些时候已经证明,早期生活压力(ES)会导致成年后的认知能力下降,这与成年海马神经发生和神经炎症的变化有关。特别是,ES 已被证明会影响神经发生率和新生细胞的存活率,并影响小胶质细胞,从而调节它们对免疫或新陈代谢挑战的反应。这两个过程都可能导致 ES 引起的认知障碍。我们和其他研究人员的新证据表明,早期营养干预可以通过营养编程防止 ES 诱导的这些影响。基于人类代谢组学研究,我们发现与咖啡有关的各种代谢物是防止人类认知能力下降的保护性分子特征的一部分。咖啡酸和绿原酸是咖啡多酚,据描述具有强大的抗氧化和抗炎作用。因此,我们在此旨在测试在早期饮食中补充咖啡酸和绿原酸是否也能保护ES诱导的认知缺陷。我们在小鼠出生后(P)第 2-9 天通过有限嵌套和铺垫范例诱导 ES。小鼠在出生后第2天开始摄入添加0.02%绿原酸(5-O-咖啡酰奎宁酸)+0.02%咖啡酸(3′,4′-二羟基肉桂酸)的食物,或在出生后第42天之前摄入对照食物。在小鼠 4 个月大时,对所有小鼠进行行为测试,并对其大脑进行染色,以检测小胶质细胞和神经发生的标记物。我们发现,在小鼠生命早期补充咖啡多酚可以防止 ES 诱导的认知缺陷,这可能是通过神经元或小胶质细胞的存活来实现的,但也可能是其他未研究的机制在起作用。这项研究为早期营养干预的潜力提供了更多支持,并强调了多酚类物质是可以防止认知能力下降的营养物质,尤其是对于暴露于 ES 的脆弱人群。
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引用次数: 0
Cross-species analysis uncovers the mitochondrial stress response in the hippocampus as a shared mechanism in mouse early life stress and human depression 跨物种分析发现海马线粒体应激反应是小鼠早期生活压力和人类抑郁症的共同机制
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-14 DOI: 10.1016/j.ynstr.2024.100643
Bente M. Hofstra , Emmy E. Hoeksema , Martien JH. Kas , Dineke S. Verbeek

Depression, or major depressive disorder, poses a significant burden for both individuals and society, affecting approximately 10.8% of the general population. This psychiatric disorder leads to approximately 800,000 deaths per year. A combination of genetic and environmental factors such as early life stress (ELS) increase the risk for development of depression in humans, and a clear role for the hippocampus in the pathophysiology of depression has been shown. Nevertheless, the underlying mechanisms of depression remain poorly understood, resulting in a lack of effective treatments. To better understand the core mechanisms underlying the development of depression, we used a cross-species design to investigate shared hippocampal pathophysiological mechanisms in mouse ELS and human depression. Mice were subjected to ELS by a maternal separation paradigm, followed by RNA sequencing analysis of the adult hippocampal tissue. This identified persistent transcriptional changes linked to mitochondrial stress response pathways, with oxidative phosphorylation and protein folding emerging as the main mechanisms affected by maternal separation. Remarkably, there was a significant overlap between the pathways involved in mitochondrial stress response we observed and publicly available RNAseq data from hippocampal tissue of depressive patients. This cross-species conservation of changes in gene expression of mitochondria-related genes suggests that mitochondrial stress may play a pivotal role in the development of depression. Our findings highlight the potential significance of the hippocampal mitochondrial stress response as a core mechanism underlying the development of depression. Further experimental investigations are required to expand our understanding of these mechanisms.

抑郁症或重度抑郁障碍给个人和社会都带来了沉重的负担,约有 10.8%的总人口受到抑郁症的影响。这种精神疾病每年导致约 80 万人死亡。遗传和环境因素(如早期生活压力(ELS))的结合增加了人类患抑郁症的风险,海马体在抑郁症的病理生理学中的作用也已得到证实。然而,人们对抑郁症的内在机制仍然知之甚少,因此缺乏有效的治疗方法。为了更好地了解抑郁症发病的核心机制,我们采用了跨物种设计来研究小鼠ELS和人类抑郁症的共同海马病理生理机制。通过母体分离范式对小鼠进行 ELS,然后对成年海马组织进行 RNA 测序分析。结果发现了与线粒体应激反应途径有关的持续转录变化,氧化磷酸化和蛋白质折叠是受母体分离影响的主要机制。值得注意的是,我们观察到的线粒体应激反应通路与从抑郁症患者海马组织中公开获得的 RNAseq 数据有明显的重叠。这种线粒体相关基因表达变化的跨物种一致性表明,线粒体应激可能在抑郁症的发病过程中起着关键作用。我们的研究结果凸显了海马线粒体应激反应作为抑郁症发病核心机制的潜在意义。我们还需要进一步的实验研究来加深对这些机制的理解。
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引用次数: 0
Neuroanatomical markers of social cognition in neglected adolescents 被忽视青少年社会认知的神经解剖标记
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-13 DOI: 10.1016/j.ynstr.2024.100642
Catalina Trujillo-Llano , Agustín Sainz-Ballesteros , Fabián Suarez-Ardila , María Luz Gonzalez-Gadea , Agustín Ibáñez , Eduar Herrera , Sandra Baez

Growing up in neglectful households can impact multiple aspects of social cognition. However, research on neglect's effects on social cognition processes and their neuroanatomical correlates during adolescence is scarce. Here, we aimed to comprehensively assess social cognition processes (recognition of basic and contextual emotions, theory of mind, the experience of envy and Schadenfreude and empathy for pain) and their structural brain correlates in adolescents with legal neglect records within family-based care. First, we compared neglected adolescents (n = 27) with control participants (n = 25) on context-sensitive social cognition tasks while controlling for physical and emotional abuse and executive and intellectual functioning. Additionally, we explored the grey matter correlates of these domains through voxel-based morphometry. Compared to controls, neglected adolescents exhibited lower performance in contextual emotional recognition and theory of mind, higher levels of envy and Schadenfreude and diminished empathy. Physical and emotional abuse and executive or intellectual functioning did not explain these effects. Moreover, social cognition scores correlated with brain volumes in regions subserving social cognition and emotional processing. Our results underscore the potential impact of neglect on different aspects of social cognition during adolescence, emphasizing the necessity for preventive and intervention strategies to address these deficits in this population.

在被忽视的家庭中成长会对社会认知的多个方面产生影响。然而,有关青少年时期忽视对社会认知过程及其神经解剖相关性的影响的研究却很少。在此,我们旨在全面评估在家庭式照料中有合法忽视记录的青少年的社会认知过程(基本情绪和情境情绪的识别、心智理论、嫉妒和幸灾乐祸的体验以及对疼痛的同理心)及其大脑结构相关性。首先,我们比较了被忽视青少年(n = 27)和对照组参与者(n = 25)在情境敏感社会认知任务上的表现,同时控制了身体和情感虐待以及执行和智力功能。此外,我们还通过体素形态计量学探讨了这些领域的灰质相关性。与对照组相比,被忽视的青少年在情境情感识别和心智理论方面表现较差,嫉妒和幸灾乐祸程度较高,移情能力较弱。身体和情感虐待以及执行或智力功能并不能解释这些影响。此外,社会认知得分与社会认知和情绪处理区域的脑容量相关。我们的研究结果凸显了青少年时期忽视对社会认知不同方面的潜在影响,强调有必要采取预防和干预策略来解决这一人群的这些缺陷。
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引用次数: 0
Neural correlates of stress-reactive rumination in depression – The role of childhood trauma and social anxiety 抑郁症患者压力反应性反刍的神经相关性--童年创伤和社交焦虑的作用
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-09 DOI: 10.1016/j.ynstr.2024.100640
David Rosenbaum , Isabell Int-Veen , Hendrik Laicher , Leonie Woloszyn , Ariane Wiegand , Sandra Ladegast , Ute Eßer , Agnes Kroczek , Daniel Sippel , Sebastian Menkor , Glenn Lawyer , Francesco Albasini , Christian Frischholz , Rainald Mössner , Vanessa Nieratschker , Elisabeth J. Leehr , Julian Rubel , Andreas J. Fallgatter , Ann-Christine Ehlis

Recent work showed an association of prefrontal dysfunctions in patients with Major Depressive Disorder (MDD) and social stress induced rumination. However, up to date it is unclear which etiological features of MDD might cause prefrontal dysfunctions. In the study at hand, we aimed to replicate recent findings, that showed prefrontal activation alterations during the Trier Social Stress Test (TSST) and subsequently increased stress-reactive rumination in MDD compared to healthy controls. Moreover, we aimed to explore the role of adverse childhood experiences and other clinical variables in this relationship. N = 55 patients currently suffering from MDD and n = 42 healthy controls (HC) underwent the TSST, while cortical activity in areas of the Cognitive Control Network (CCN) was measured via functional near-infrared spectroscopy (fNIRS). The TSST successfully induced a stress reaction (physiologically, as well as indicated by subjective stress ratings) and state rumination in all subjects with moderate to large effect sizes. In comparison to HC, MDD patients showed elevated levels of state rumination with large effect sizes, as well as a typical pattern of reduced cortical oxygenation during stress in the CCN with moderate effect sizes. Self-reported emotional abuse and social anxiety were moderately positively associated with increased stress-reactive rumination. Within the MDD sample, emotional abuse was negatively and social anxiety positively associated with cortical oxygenation within the CCN with moderate to large effect sizes. In conclusion, our results replicate previous findings on MDD-associated prefrontal hypoactivity during stress and extends the research toward specific subtypes of depression.

最近的研究表明,重度抑郁症(MDD)患者的前额叶功能障碍与社会压力引起的反刍有关。然而,迄今为止,尚不清楚 MDD 的哪些病因特征可能会导致前额叶功能障碍。与健康对照组相比,特里尔社会压力测试(TSST)显示 MDD 患者在测试过程中前额叶激活发生改变,随后压力反应性反刍增加。此外,我们还旨在探索不良童年经历和其他临床变量在这种关系中的作用。55 名 MDD 患者和 42 名健康对照者(HC)接受了 TSST 测试,同时通过功能性近红外光谱(fNIRS)测量了认知控制网络(CCN)区域的皮层活动。TSST 成功地诱发了所有受试者的应激反应(生理反应以及主观应激评分)和状态反刍,并产生了中等到较大的效应量。与HC相比,MDD患者的状态反刍水平升高,影响程度较大;在CCN中,患者在应激时皮层氧合降低,影响程度中等。自我报告的情感虐待和社交焦虑与压力反应性反刍的增加呈中度正相关。在 MDD 样本中,情感虐待与 CCN 中的皮质氧合呈负相关,社交焦虑与 CCN 中的皮质氧合呈正相关,效应大小为中等到较大。总之,我们的研究结果重复了之前关于 MDD 相关前额叶在应激时活性低下的发现,并将研究扩展到了特定的抑郁症亚型。
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引用次数: 0
Toll-like receptor 7: A novel neuroimmune target to reduce excessive alcohol consumption Toll 样受体 7:减少过度饮酒的新型神经免疫靶标
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-06 DOI: 10.1016/j.ynstr.2024.100639
Ruth L. Allard , Jody Mayfield , Riccardo Barchiesi , Nihal A. Salem , R. Dayne Mayfield

Toll-like receptors (TLRs) are a family of innate immune receptors that recognize molecular patterns in foreign pathogens and intrinsic danger/damage signals from cells. TLR7 is a nucleic acid sensing endosomal TLR that is activated by single-stranded RNAs from microbes or by small noncoding RNAs that act as endogenous ligands. TLR7 signals through the MyD88 adaptor protein and activates the transcription factor interferon regulatory factor 7 (IRF7). TLR7 is found throughout the brain and is highly expressed in microglia, the main immune cells of the brain that have also been implicated in alcohol drinking in mice. Upregulation of TLR7 mRNA and protein has been identified in postmortem hippocampus and cortex from AUD subjects that correlated positively with lifetime consumption of alcohol. Similarly, Tlr7 and downstream signaling genes were upregulated in rat hippocampal and cortical slice cultures after chronic alcohol exposure and in these regions after chronic binge-like alcohol treatment in mice. In addition, repeated administration of the synthetic TLR7 agonists imiquimod (R837) or resiquimod (R848) increased voluntary alcohol drinking in different rodent models and produced sustained upregulation of IRF7 in the brain. These findings suggest that chronic TLR7 activation may drive excessive alcohol drinking. In the brain, this could occur through increased levels of endogenous TLR7 activators, like microRNAs and Y RNAs. This review explores chronic TLR7 activation as a pathway of dysregulated neuroimmune signaling in AUD and the endogenous small RNA ligands in the brain that could perpetuate innate immune responses and escalate alcohol drinking.

Toll 样受体(TLRs)是先天性免疫受体的一个家族,可识别外来病原体的分子模式和细胞的内在危险/损伤信号。TLR7 是一种核酸感应内体 TLR,可被微生物的单链 RNA 或作为内源配体的小型非编码 RNA 激活。TLR7 通过 MyD88 适配蛋白发出信号,并激活转录因子干扰素调节因子 7(IRF7)。TLR7 存在于整个大脑中,并在小胶质细胞中高度表达,小胶质细胞是大脑的主要免疫细胞,也与小鼠饮酒有关。在 AUD 受试者死后的海马和皮层中发现了 TLR7 mRNA 和蛋白质的上调,这与终生饮酒量呈正相关。同样,大鼠海马和大脑皮层切片培养物在长期暴露于酒精后,以及小鼠长期酗酒后,Tlr7 和下游信号基因也会上调。此外,在不同的啮齿动物模型中,重复给予合成的 TLR7 激动剂咪喹莫特(R837)或瑞喹莫特(R848)会增加自愿饮酒,并在大脑中产生持续的 IRF7 上调。这些研究结果表明,慢性 TLR7 激活可能会导致过度饮酒。在大脑中,这可能是通过内源性 TLR7 激活剂(如 microRNA 和 Y RNA)水平的增加而发生的。本综述探讨了慢性 TLR7 激活作为 AUD 神经免疫信号传导失调的途径,以及大脑中可能使先天性免疫反应和饮酒升级永久化的内源性小 RNA 配体。
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引用次数: 0
Subcallosal area 25: Its responsivity to the stress hormone cortisol and its opposing effects on appetitive motivation in marmosets 丘脑下 25 区:它对压力荷尔蒙皮质醇的反应及其对狨猴食欲动机的相反影响
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-01 DOI: 10.1016/j.ynstr.2024.100637
Rana Banai Tizkar, Lauren McIver, Christian Michael Wood , Angela Charlotte Roberts

Aberrant activity in caudal subcallosal anterior cingulate cortex (scACC) is implicated in depression and anxiety symptomatology, with its normalisation a putative biomarker of successful treatment response. The function of scACC in emotion processing and mental health is not fully understood despite its known influence on stress-mediated processes through its rich expression of mineralocorticoid and glucocorticoid receptors. Here we examine the causal interaction between area 25 within scACC (scACC-25) and the stress hormone, cortisol, in the context of anhedonia and anxiety-like behaviour. In addition, the overall role of scACC-25 in hedonic capacity and motivation is investigated under transient pharmacological inactivation and overactivation. The results suggest that a local increase of cortisol in scACC-25 shows a rapid induction of anticipatory anhedonia and increased responsiveness to uncertain threat. Separate inactivation and overactivation of scACC-25 increased and decreased motivation and hedonic capacity, respectively, likely through different underlying mechanisms. Together, these data show that area scACC-25 has a causal role in consummatory and motivational behaviour and produces rapid responses to the stress hormone cortisol, that mediates anhedonia and anxiety-like behaviour.

胼胝体尾下前扣带回皮层(scACC)的异常活动与抑郁和焦虑症状有关,其正常化是成功治疗反应的潜在生物标志物。尽管人们知道扣带回皮质通过其丰富的矿物质皮质激素和糖皮质激素受体的表达对压力介导的过程产生影响,但它在情绪处理和心理健康中的功能尚未完全明了。在此,我们研究了scACC内的25区(scACC-25)与应激激素皮质醇之间在失神和焦虑样行为方面的因果相互作用。此外,我们还研究了在瞬时药理失活和过度失活的情况下,scACC-25 在享乐能力和动机中的整体作用。结果表明,scACC-25 中皮质醇的局部增加会迅速诱发预期性失神和对不确定威胁的反应性增加。scACC-25的单独失活和过度失活分别增加和减少了动机和享乐能力,这可能是通过不同的潜在机制实现的。这些数据共同表明,scACC-25区域在消费行为和动机行为中起着因果作用,并对压力荷尔蒙皮质醇产生快速反应,从而介导失乐症和焦虑样行为。
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引用次数: 0
Corrigendum to “Cross-sectional study of retrospective self-reported childhood emotional neglect and inhibitory neurometabolite levels in the pregenual anterior cingulate cortex in adult humans” [Neurobiol. Stress, 25 (July 2023), 100556] 对 "回顾性自我报告的童年情感忽视与成人前扣带回皮层抑制性神经代谢物水平的横断面研究 "的更正,《压力神经生物学》,第 25 卷,2023 年 7 月,100556 页
IF 5 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-01 DOI: 10.1016/j.ynstr.2024.100630
Luisa Herrmann , Johanna Ade , Anne Kühnel , Annina Widmann , Liliana Ramona Demenescu , Meng Li , Nils Opel , Oliver Speck , Martin Walter , Lejla Colic
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引用次数: 0
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Neurobiology of Stress
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