首页 > 最新文献

Neurobiology of Stress最新文献

英文 中文
Predator odor stress reactivity, alcohol drinking and the endocannabinoid system 捕食者气味应激反应、饮酒和内源性大麻素系统
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-04-04 DOI: 10.1016/j.ynstr.2024.100634
Laura C. Ornelas , Joyce Besheer

Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are highly comorbid and individual differences in response to stress suggest resilient and susceptible populations. Using animal models to target neurobiological mechanisms associated with individual variability in stress coping responses and the relationship with subsequent increases in alcohol consumption has important implications for the field of traumatic stress and alcohol disorders. The current review discusses the unique advantages of utilizing predator odor stressor exposure models, specifically using 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) on better understanding PTSD pathophysiology and neurobiological mechanisms associated with stress reactivity and subsequent increases in alcohol drinking. Furthermore, there has been increasing interest regarding the role of the endocannabinoid system in modulating behavioral responses to stress with an emphasis on stress coping and individual differences in stress-susceptibility. Therefore, the current review focuses on the topic of endocannabinoid modulation of stress reactive behaviors during and after exposure to a predator odor stressor, with implications on modulating distinctly different behavioral coping strategies.

创伤后应激障碍(PTSD)和酒精使用障碍(AUD)是高度并发症,对应激反应的个体差异表明有适应能力的人群和易受影响的人群。利用动物模型瞄准与压力应对反应个体差异相关的神经生物学机制以及与随后酒精消费增加的关系,对创伤应激障碍和酒精紊乱领域具有重要意义。本综述讨论了利用捕食者气味应激源暴露模型的独特优势,特别是利用 2,5-二氢-2,4,5-三甲基噻唑啉(TMT)来更好地了解创伤后应激障碍的病理生理学以及与应激反应性和随后的饮酒增加有关的神经生物学机制。此外,人们越来越关注内源性大麻素系统在调节应激行为反应中的作用,重点是应激应对和应激易感性的个体差异。因此,本综述将重点放在内源性大麻素对暴露于捕食者气味应激源期间和之后的应激反应行为的调节作用,以及对调节截然不同的行为应对策略的影响。
{"title":"Predator odor stress reactivity, alcohol drinking and the endocannabinoid system","authors":"Laura C. Ornelas ,&nbsp;Joyce Besheer","doi":"10.1016/j.ynstr.2024.100634","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100634","url":null,"abstract":"<div><p>Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are highly comorbid and individual differences in response to stress suggest resilient and susceptible populations. Using animal models to target neurobiological mechanisms associated with individual variability in stress coping responses and the relationship with subsequent increases in alcohol consumption has important implications for the field of traumatic stress and alcohol disorders. The current review discusses the unique advantages of utilizing predator odor stressor exposure models, specifically using 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) on better understanding PTSD pathophysiology and neurobiological mechanisms associated with stress reactivity and subsequent increases in alcohol drinking. Furthermore, there has been increasing interest regarding the role of the endocannabinoid system in modulating behavioral responses to stress with an emphasis on stress coping and individual differences in stress-susceptibility. Therefore, the current review focuses on the topic of endocannabinoid modulation of stress reactive behaviors during and after exposure to a predator odor stressor, with implications on modulating distinctly different behavioral coping strategies.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100634"},"PeriodicalIF":5.0,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000304/pdfft?md5=16a71c61b882ebcace38c109e1ef6837&pid=1-s2.0-S2352289524000304-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140535647","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
Effects of autotaxin and lysophosphatidic acid deficiencies on depression-like behaviors in mice exposed to chronic unpredictable mild stress 自体促肾上腺皮质激素和溶血磷脂酸缺乏症对长期暴露于不可预测的轻度应激的小鼠抑郁样行为的影响
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-04-04 DOI: 10.1016/j.ynstr.2024.100632
Chao Wang , Ningyuan Li , Yuqi Feng , Siqi Sun , Jingtong Rong , Xin-hui Xie , Shuxian Xu , Zhongchun Liu

The involvement of lipids in the mechanism of depression has triggered extensive discussions. Earlier studies have identified diminished levels of lysophosphatidic acid (LPA) and autotaxin (ATX) in individuals experiencing depression. However, the exact significance of this phenomenon in relation to depression remains inconclusive. This study seeks to explore the deeper implications of these observations. We assessed alterations in ATX and LPA in both the control group and the chronic unpredictable mild stress (CUMS) model group. Additionally, the impact of ATX adeno-associated virus (AAV-ATX) injection into the hippocampus was validated through behavioral tests in CUMS-exposed mice. Furthermore, we probed the effects of LPA on synapse-associated proteins both in HT22 cells and within the mouse hippocampus. The mechanisms underpinning the LPA-triggered shifts in protein expression were further scrutinized. Hippocampal tissues were augmented with ATX to assess its potential to alleviate depression-like behavior by modulating synaptic-related proteins. Our findings suggest that the decrement in ATX and LPA levels alters the expression of proteins associated with synaptic plasticity in vitro and in vivo, such as synapsin-I (SYN), synaptophysin (SYP), and brain-derived neurotrophic factor (BDNF). Moreover, we discerned a role for the ERK/CREB signaling pathway in mediating the effects of ATX and LPA. Importantly, strategic supplementation of ATX effectively mitigated depression-like behaviors. This study indicates that the ATX-LPA pathway may influence depression-like behaviors by modulating synaptic plasticity in the brains of CUMS-exposed mice. These insights augment our understanding of depression's potential pathogenic mechanism in the context of lipid metabolism and propose promising therapeutic strategies for ameliorating the disease.

脂质参与抑郁症的机理引发了广泛的讨论。早期的研究发现,抑郁症患者体内溶血磷脂酸(LPA)和自体免疫球蛋白(ATX)的水平降低。然而,这一现象对抑郁症的确切意义仍无定论。本研究试图探索这些观察结果的深层含义。我们评估了对照组和慢性不可预测轻度应激(CUMS)模型组中 ATX 和 LPA 的变化。此外,我们还通过对暴露于 CUMS 的小鼠进行行为测试,验证了向海马注射 ATX 腺相关病毒(AAV-ATX)的影响。此外,我们还探究了LPA对HT22细胞和小鼠海马内突触相关蛋白的影响。我们还进一步研究了 LPA 触发蛋白质表达变化的机制。用 ATX 增强海马组织,以评估其通过调节突触相关蛋白来减轻抑郁样行为的潜力。我们的研究结果表明,ATX和LPA水平的降低会改变体外和体内与突触可塑性相关的蛋白质的表达,如突触素I(SYN)、突触素(SYP)和脑源性神经营养因子(BDNF)。此外,我们还发现ERK/CREB 信号通路在介导 ATX 和 LPA 的作用方面发挥了作用。重要的是,战略性地补充 ATX 能有效缓解抑郁样行为。这项研究表明,ATX-LPA通路可能通过调节CUMS暴露小鼠大脑的突触可塑性来影响抑郁样行为。这些见解加深了我们对脂质代谢背景下抑郁症潜在致病机制的理解,并为改善这种疾病提出了有前景的治疗策略。
{"title":"Effects of autotaxin and lysophosphatidic acid deficiencies on depression-like behaviors in mice exposed to chronic unpredictable mild stress","authors":"Chao Wang ,&nbsp;Ningyuan Li ,&nbsp;Yuqi Feng ,&nbsp;Siqi Sun ,&nbsp;Jingtong Rong ,&nbsp;Xin-hui Xie ,&nbsp;Shuxian Xu ,&nbsp;Zhongchun Liu","doi":"10.1016/j.ynstr.2024.100632","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100632","url":null,"abstract":"<div><p>The involvement of lipids in the mechanism of depression has triggered extensive discussions. Earlier studies have identified diminished levels of lysophosphatidic acid (LPA) and autotaxin (ATX) in individuals experiencing depression. However, the exact significance of this phenomenon in relation to depression remains inconclusive. This study seeks to explore the deeper implications of these observations. We assessed alterations in ATX and LPA in both the control group and the chronic unpredictable mild stress (CUMS) model group. Additionally, the impact of ATX adeno-associated virus (AAV-ATX) injection into the hippocampus was validated through behavioral tests in CUMS-exposed mice. Furthermore, we probed the effects of LPA on synapse-associated proteins both in HT22 cells and within the mouse hippocampus. The mechanisms underpinning the LPA-triggered shifts in protein expression were further scrutinized. Hippocampal tissues were augmented with ATX to assess its potential to alleviate depression-like behavior by modulating synaptic-related proteins. Our findings suggest that the decrement in ATX and LPA levels alters the expression of proteins associated with synaptic plasticity <em>in vitro</em> and <em>in vivo</em>, such as synapsin-I (SYN), synaptophysin (SYP), and brain-derived neurotrophic factor (BDNF). Moreover, we discerned a role for the ERK/CREB signaling pathway in mediating the effects of ATX and LPA. Importantly, strategic supplementation of ATX effectively mitigated depression-like behaviors. This study indicates that the ATX-LPA pathway may influence depression-like behaviors by modulating synaptic plasticity in the brains of CUMS-exposed mice. These insights augment our understanding of depression's potential pathogenic mechanism in the context of lipid metabolism and propose promising therapeutic strategies for ameliorating the disease.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100632"},"PeriodicalIF":5.0,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000286/pdfft?md5=bb6f02b88dbf02788d634a75b6124607&pid=1-s2.0-S2352289524000286-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140345221","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
CRF binding protein activity in the hypothalamic paraventricular nucleus is essential for stress adaptations and normal maternal behaviour in lactating rats 下丘脑室旁核的 CRF 结合蛋白活性对哺乳期大鼠的应激适应和正常母性行为至关重要
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-27 DOI: 10.1016/j.ynstr.2024.100631
Alice Sanson , Paula Krieg , Milena M. Schramm , Kerstin Kellner , Rodrigue Maloumby , Stefanie M. Klampfl , Paula J. Brunton , Oliver J. Bosch

To ensure the unrestricted expression of maternal behaviour peripartum, activity of the corticotropin-releasing factor (CRF) system needs to be minimised. CRF binding protein (CRF-BP) might be crucial for this adaptation, as its primary function is to sequester freely available CRF and urocortin1, thereby dampening CRF receptor (CRF-R) signalling. So far, the role of CRF-BP in the maternal brain has barely been studied, and a potential role in curtailing activation of the stress axis is unknown.

We studied gene expression for CRF-BP and both CRF-R within the paraventricular nucleus (PVN) of the hypothalamus. In lactating rats, Crh-bp expression in the parvocellular PVN was significantly higher and Crh-r1 expression in the PVN significantly lower compared to virgin rats. Acute CRF-BP inhibition in the PVN with infusion of CRF(6–33) increased basal plasma corticosterone concentrations under unstressed conditions in dams. Furthermore, while acute intra-PVN infusion of CRF increased corticosterone secretion in virgin rats, it was ineffective in vehicle (VEH)-pre-treated lactating rats, probably due to a buffering effect of CRF-BP. Indeed, pre-treatment with CRF(6–33) reinstated a corticosterone response to CRF in lactating rats, highlighting the critical role of CRF-BP in maintaining attenuated stress reactivity in lactation. To our knowledge, this is the first study linking hypothalamic CRF-BP activity to hypothalamic-pituitary-adrenal axis regulation in lactation. In terms of behaviour, acute CRF-BP inhibition in the PVN under non-stress conditions reduced blanket nursing 60 min and licking/grooming 90 min after infusion compared to VEH-treated rats, while increasing maternal aggression towards an intruder. Lastly, chronic intra-PVN inhibition of CRF-BP strongly reduced maternal aggression, with modest effects on maternal motivation and care.

Taken together, intact activity of the CRF-BP in the PVN during the postpartum period is essential for the dampened responsiveness of the stress axis, as well as for the full expression of appropriate maternal behaviour.

为了确保围产期母性行为的不受限制表达,需要尽量减少促肾上腺皮质激素释放因子(CRF)系统的活动。CRF结合蛋白(CRF-BP)可能是这种适应的关键,因为它的主要功能是封闭可自由利用的CRF和尿皮质素1,从而抑制CRF受体(CRF-R)的信号传导。我们研究了下丘脑室旁核(PVN)中 CRF-BP 和 CRF-R 的基因表达。与原始大鼠相比,哺乳大鼠下丘脑室旁核(PVN)中Crh-bp的表达明显较高,而Crh-r1的表达则明显较低。通过输注 CRF(6-33)抑制 PVN 中的急性 CRF-BP,可增加母鼠在非应激条件下的基础血浆皮质酮浓度。此外,虽然在PVN内急性输注CRF可增加处女大鼠的皮质酮分泌,但对经车辆(VEH)预处理的泌乳大鼠却无效,这可能是由于CRF-BP的缓冲作用。事实上,CRF(6-33)的预处理恢复了哺乳期大鼠对CRF的皮质酮反应,突出了CRF-BP在维持哺乳期应激反应减弱中的关键作用。据我们所知,这是首次将哺乳期下丘脑 CRF-BP 活性与下丘脑-垂体-肾上腺轴调节联系起来的研究。在行为方面,与 VEH 处理的大鼠相比,非应激条件下 PVN 内的急性 CRF-BP 抑制减少了输注后 60 分钟的空白哺乳和 90 分钟的舔舐/梳理,同时增加了母体对入侵者的攻击性。总之,在产后期间,PVN 中 CRF-BP 的完整活性对于抑制应激轴的反应以及充分表达适当的母性行为至关重要。
{"title":"CRF binding protein activity in the hypothalamic paraventricular nucleus is essential for stress adaptations and normal maternal behaviour in lactating rats","authors":"Alice Sanson ,&nbsp;Paula Krieg ,&nbsp;Milena M. Schramm ,&nbsp;Kerstin Kellner ,&nbsp;Rodrigue Maloumby ,&nbsp;Stefanie M. Klampfl ,&nbsp;Paula J. Brunton ,&nbsp;Oliver J. Bosch","doi":"10.1016/j.ynstr.2024.100631","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100631","url":null,"abstract":"<div><p>To ensure the unrestricted expression of maternal behaviour peripartum, activity of the corticotropin-releasing factor (CRF) system needs to be minimised. CRF binding protein (CRF-BP) might be crucial for this adaptation, as its primary function is to sequester freely available CRF and urocortin1, thereby dampening CRF receptor (CRF-R) signalling. So far, the role of CRF-BP in the maternal brain has barely been studied, and a potential role in curtailing activation of the stress axis is unknown.</p><p>We studied gene expression for CRF-BP and both CRF-R within the paraventricular nucleus (PVN) of the hypothalamus. In lactating rats, <em>Crh-bp</em> expression in the parvocellular PVN was significantly higher and <em>Crh-r1</em> expression in the PVN significantly lower compared to virgin rats. Acute CRF-BP inhibition in the PVN with infusion of CRF(6–33) increased basal plasma corticosterone concentrations under unstressed conditions in dams. Furthermore, while acute intra-PVN infusion of CRF increased corticosterone secretion in virgin rats, it was ineffective in vehicle (VEH)-pre-treated lactating rats, probably due to a buffering effect of CRF-BP. Indeed, pre-treatment with CRF(6–33) reinstated a corticosterone response to CRF in lactating rats, highlighting the critical role of CRF-BP in maintaining attenuated stress reactivity in lactation. To our knowledge, this is the first study linking hypothalamic CRF-BP activity to hypothalamic-pituitary-adrenal axis regulation in lactation. In terms of behaviour, acute CRF-BP inhibition in the PVN under non-stress conditions reduced blanket nursing 60 min and licking/grooming 90 min after infusion compared to VEH-treated rats, while increasing maternal aggression towards an intruder. Lastly, chronic intra-PVN inhibition of CRF-BP strongly reduced maternal aggression, with modest effects on maternal motivation and care.</p><p>Taken together, intact activity of the CRF-BP in the PVN during the postpartum period is essential for the dampened responsiveness of the stress axis, as well as for the full expression of appropriate maternal behaviour.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100631"},"PeriodicalIF":5.0,"publicationDate":"2024-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000274/pdfft?md5=01b24c39ff506e14f0e16b63b2cdff87&pid=1-s2.0-S2352289524000274-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140345438","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
Emotional abuse mediated by negative automatic thoughts impacts functional connectivity during adolescence 以消极的自动想法为中介的情感虐待影响青春期的功能连通性
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-19 DOI: 10.1016/j.ynstr.2024.100623
Dageon Yeo , Seulgi Lee , Haemi Choi , Min-Hyeon Park , Bumhee Park

Background

Emotional abuse during childhood and adolescence is thought to be associated with the brain; however, the neural mechanism underlying the cognitive process remains unknown. Therefore, we aimed to investigate the mediating effect of negative automatic thoughts on the relationship between emotional abuse and resting-state functional connectivity (rsFC) during adolescence.

Method

Our community sample included 54 adolescents aged 13–17 years in the statistical analysis. Resting-state functional and structural magnetic resonance imaging (MRI) was performed, while emotional abuse and negative automatic thoughts were assessed using self-reported scales. A mediation analysis was used to assess the contributions of early traumatic events and negative automatic thoughts to resting functional connectivity.

Result

Higher negative automatic thoughts were associated with lower connectivity in the context of greater emotional abuse (i.e., suppression effect). Thus, the relationships between emotional abuse and connectivity in the precuneus (pCun)-medial prefrontal cortex, parahippocampal cortex-extrastriate cortex, and temporal cortex-temporal pole were decreased by negative automatic thoughts. In contrast, functional connections in the pCun-pCun, pCun-precuneus/posterior cingulate cortex, and nucleus accumbens-somatomotor areas were strongly mediated when emotionally abused adolescents reported a high tendency for negative automatic thoughts.

Conclusion

Negative automatic thoughts strengthened the relationship between emotional abuse and rsFC. These findings highlight the underlying cognitive processing of the traumatic event-neural system, supporting the use of cognitive therapy for post-traumatic symptoms.

背景人们认为童年和青少年时期的情感虐待与大脑有关;然而,这一认知过程的神经机制仍然未知。因此,我们旨在研究消极自动想法对青春期情感虐待与静息态功能连通性(rsFC)之间关系的中介作用。我们对54名13-17岁的青少年进行了社区样本统计分析,并进行了静息状态功能和结构磁共振成像(MRI)检查,同时使用自我报告量表对情感虐待和消极自动想法进行了评估。结果较高的消极自动想法与较低的连接性有关,而较高的情绪虐待程度则与较低的连接性有关(即抑制效应)。因此,情绪虐待与楔前皮层(pCun)-内侧前额叶皮层、海马旁皮层-外显皮层和颞皮层-颞极的连接性之间的关系因消极自动想法而降低。与此相反,当遭受情感虐待的青少年报告其有较高的消极自动想法倾向时,pCun-pCun、pCun-precuneus/后扣带回皮层和伏隔核-躯体运动区的功能连接则会受到强烈的介导。这些发现强调了创伤事件-神经系统的潜在认知处理过程,支持使用认知疗法治疗创伤后症状。
{"title":"Emotional abuse mediated by negative automatic thoughts impacts functional connectivity during adolescence","authors":"Dageon Yeo ,&nbsp;Seulgi Lee ,&nbsp;Haemi Choi ,&nbsp;Min-Hyeon Park ,&nbsp;Bumhee Park","doi":"10.1016/j.ynstr.2024.100623","DOIUrl":"10.1016/j.ynstr.2024.100623","url":null,"abstract":"<div><h3>Background</h3><p>Emotional abuse during childhood and adolescence is thought to be associated with the brain; however, the neural mechanism underlying the cognitive process remains unknown. Therefore, we aimed to investigate the mediating effect of negative automatic thoughts on the relationship between emotional abuse and resting-state functional connectivity (rsFC) during adolescence.</p></div><div><h3>Method</h3><p>Our community sample included 54 adolescents aged 13–17 years in the statistical analysis. Resting-state functional and structural magnetic resonance imaging (MRI) was performed, while emotional abuse and negative automatic thoughts were assessed using self-reported scales. A mediation analysis was used to assess the contributions of early traumatic events and negative automatic thoughts to resting functional connectivity.</p></div><div><h3>Result</h3><p>Higher negative automatic thoughts were associated with lower connectivity in the context of greater emotional abuse (i.e., suppression effect). Thus, the relationships between emotional abuse and connectivity in the precuneus (pCun)-medial prefrontal cortex, parahippocampal cortex-extrastriate cortex, and temporal cortex-temporal pole were decreased by negative automatic thoughts. In contrast, functional connections in the pCun-pCun, pCun-precuneus/posterior cingulate cortex, and nucleus accumbens-somatomotor areas were strongly mediated when emotionally abused adolescents reported a high tendency for negative automatic thoughts.</p></div><div><h3>Conclusion</h3><p>Negative automatic thoughts strengthened the relationship between emotional abuse and rsFC. These findings highlight the underlying cognitive processing of the traumatic event-neural system, supporting the use of cognitive therapy for post-traumatic symptoms.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100623"},"PeriodicalIF":5.0,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000195/pdfft?md5=fd150258965cc78c588b6f633393a85c&pid=1-s2.0-S2352289524000195-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140278995","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
A gut (microbiome) feeling about addiction: Interactions with stress and social systems 特约评论--"压力与酒精 "特刊:关于成瘾的直觉(微生物组)感受:与压力和社会系统的相互作用
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-18 DOI: 10.1016/j.ynstr.2024.100629
Rubén García-Cabrerizo , John F. Cryan

In recent years, an increasing attention has given to the intricate and diverse connection of microorganisms residing in our gut and their impact on brain health and central nervous system disease. There has been a shift in mindset to understand that drug addiction is not merely a condition that affects the brain, it is now being recognized as a disorder that also involves external factors such as the intestinal microbiota, which could influence vulnerability and the development of addictive behaviors. Furthermore, stress and social interactions, which are closely linked to the intestinal microbiota, are powerful modulators of addiction. This review delves into the mechanisms through which the microbiota-stress-immune axis may shape drug addiction and social behaviors. This work integrates preclinical and clinical evidence that demonstrate the bidirectional communication between stress, social behaviors, substance use disorders and the gut microbiota, suggesting that gut microbes might modulate social stress having a significance in drug addiction.

近年来,人们越来越关注居住在我们肠道中的微生物之间错综复杂、多种多样的联系,以及它们对大脑健康和中枢神经系统疾病的影响。人们已经转变了观念,认识到吸毒上瘾不仅仅是一种影响大脑的疾病,它现在被认为是一种疾病,还涉及肠道微生物群等外部因素,这些因素可能会影响易感性和成瘾行为的发展。此外,与肠道微生物群密切相关的压力和社会互动也是成瘾的强大调节因素。这篇综述深入探讨了微生物群-压力-免疫轴可能影响药物成瘾和社会行为的机制。这项工作综合了临床前和临床证据,证明了压力、社会行为、药物使用障碍和肠道微生物群之间的双向交流,表明肠道微生物可能调节社会压力,对药物成瘾具有重要意义。
{"title":"A gut (microbiome) feeling about addiction: Interactions with stress and social systems","authors":"Rubén García-Cabrerizo ,&nbsp;John F. Cryan","doi":"10.1016/j.ynstr.2024.100629","DOIUrl":"10.1016/j.ynstr.2024.100629","url":null,"abstract":"<div><p>In recent years, an increasing attention has given to the intricate and diverse connection of microorganisms residing in our gut and their impact on brain health and central nervous system disease. There has been a shift in mindset to understand that drug addiction is not merely a condition that affects the brain, it is now being recognized as a disorder that also involves external factors such as the intestinal microbiota, which could influence vulnerability and the development of addictive behaviors. Furthermore, stress and social interactions, which are closely linked to the intestinal microbiota, are powerful modulators of addiction. This review delves into the mechanisms through which the microbiota-stress-immune axis may shape drug addiction and social behaviors. This work integrates preclinical and clinical evidence that demonstrate the bidirectional communication between stress, social behaviors, substance use disorders and the gut microbiota, suggesting that gut microbes might modulate social stress having a significance in drug addiction.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100629"},"PeriodicalIF":5.0,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000250/pdfft?md5=9ba60fdcad00dec74375cbdfd4d053e9&pid=1-s2.0-S2352289524000250-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140153852","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
β1-adrenoceptor expression on GABAergic interneurons in primate dorsolateral prefrontal cortex: potential role in stress-induced cognitive dysfunction 灵长类背外侧前额叶皮层 GABA 能中间神经元上的β1-肾上腺素受体表达:在压力诱导的认知功能障碍中的潜在作用
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-15 DOI: 10.1016/j.ynstr.2024.100628
M.K.P. Joyce, S. Yang, K. Morin, A. Duque, J. Arellano, D. Datta, M. Wang, A.F.T. Arnsten

Uncontrollable stress exposure impairs working memory and reduces the firing of dorsolateral prefrontal cortex (dlPFC) “Delay cells”, involving high levels of norepinephrine and dopamine release. Previous work has focused on catecholamine actions on dlPFC pyramidal cells, but inhibitory interneurons may contribute as well. The current study combined immunohistochemistry and multi-scale microscopy with iontophoretic physiology and behavioral analyses to examine the effects of beta1-noradrenergic receptors (β1-ARs) on inhibitory neurons in layer III dlPFC. We found β1-AR robustly expressed on different classes of inhibitory neurons labeled by the calcium-binding proteins calbindin (CB), calretinin (CR), and parvalbumin (PV). Immunoelectron microscopy confirmed β1-AR expression on the plasma membrane of PV-expressing dendrites. PV interneurons can be identified as fast-spiking (FS) in physiological recordings, and thus were studied in macaques performing a working memory task. Iontophoresis of a β1-AR agonist had a mixed effect, increasing the firing of a subset and decreasing the firing of others, likely reflecting loss of firing of the entire microcircuit. This loss of overall firing likely contributes to impaired working memory during stress, as pretreatment with the selective β1-AR antagonist, nebivolol, prevented stress-induced working memory deficits. Thus, selective β1-AR antagonists may be helpful in treating stress-related disorders.

无法控制的压力会损害工作记忆,并降低背外侧前额叶皮层(dlPFC)"延迟细胞 "的发射,这涉及到高水平的去甲肾上腺素和多巴胺释放。以前的研究主要关注儿茶酚胺对前额叶皮质锥体细胞的作用,但抑制性中间神经元也可能起作用。本研究将免疫组化、多尺度显微镜、离子渗透生理学和行为分析结合起来,研究了β1-去甲肾上腺素能受体(β1-ARs)对第III层dlPFC抑制性神经元的影响。我们发现β1-AR在不同类别的抑制性神经元上都有很强的表达,这些抑制性神经元由钙结合蛋白钙宾蛋白(CB)、钙视蛋白(CR)和钙旁蛋白(PV)标记。免疫电镜证实,β1-AR 在 PV 表达树突的质膜上表达。在生理记录中,PV 中间神经元可被识别为快速尖峰(FS),因此在猕猴执行工作记忆任务时对其进行了研究。对β1-AR激动剂进行离子注入会产生混合效应,增加一个子集的点燃,减少其他子集的点燃,这可能反映了整个微电路点燃的丧失。这种整体发射损失可能是应激时工作记忆受损的原因之一,因为使用选择性β1-AR拮抗剂奈必洛尔进行预处理可防止应激引起的工作记忆缺陷。因此,选择性β1-AR拮抗剂可能有助于治疗应激相关疾病。
{"title":"β1-adrenoceptor expression on GABAergic interneurons in primate dorsolateral prefrontal cortex: potential role in stress-induced cognitive dysfunction","authors":"M.K.P. Joyce,&nbsp;S. Yang,&nbsp;K. Morin,&nbsp;A. Duque,&nbsp;J. Arellano,&nbsp;D. Datta,&nbsp;M. Wang,&nbsp;A.F.T. Arnsten","doi":"10.1016/j.ynstr.2024.100628","DOIUrl":"10.1016/j.ynstr.2024.100628","url":null,"abstract":"<div><p>Uncontrollable stress exposure impairs working memory and reduces the firing of dorsolateral prefrontal cortex (dlPFC) “Delay cells”, involving high levels of norepinephrine and dopamine release. Previous work has focused on catecholamine actions on dlPFC pyramidal cells, but inhibitory interneurons may contribute as well. The current study combined immunohistochemistry and multi-scale microscopy with iontophoretic physiology and behavioral analyses to examine the effects of beta1-noradrenergic receptors (β1-ARs) on inhibitory neurons in layer III dlPFC. We found β1-AR robustly expressed on different classes of inhibitory neurons labeled by the calcium-binding proteins calbindin (CB), calretinin (CR), and parvalbumin (PV). Immunoelectron microscopy confirmed β1-AR expression on the plasma membrane of PV-expressing dendrites. PV interneurons can be identified as fast-spiking (FS) in physiological recordings, and thus were studied in macaques performing a working memory task. Iontophoresis of a β1-AR agonist had a mixed effect, increasing the firing of a subset and decreasing the firing of others, likely reflecting loss of firing of the entire microcircuit. This loss of overall firing likely contributes to impaired working memory during stress, as pretreatment with the selective β1-AR antagonist, nebivolol, prevented stress-induced working memory deficits. Thus, selective β1-AR antagonists may be helpful in treating stress-related disorders.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100628"},"PeriodicalIF":5.0,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000249/pdfft?md5=46d28d2d6f2a21c3801598b596f48a07&pid=1-s2.0-S2352289524000249-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140154008","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
Astrocyte focal adhesion kinase reduces passive stress coping by inhibiting ciliary neurotrophic factor only in female mice 星形胶质细胞局灶粘附激酶仅通过抑制睫状神经营养因子降低雌性小鼠的被动压力应对能力
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-11 DOI: 10.1016/j.ynstr.2024.100621
Cuihong Jia, W. Drew Gill, Chiharu Lovins, Russell W. Brown , Theo Hagg

Astrocytes have been implicated in stress responses and produce ciliary neurotrophic factor (CNTF), which we have shown in the mouse medial amygdala (MeA) to promote passive stress coping response only in females. Pharmacological inhibition of focal adhesion kinase (FAK) upregulates CNTF expression. Here, we found that inducible knockout of FAK in astrocytes or systemic treatment with an FAK inhibitor increased passive coping behavior, i.e., immobility, in an acute forced swim stress test in female, but not male, mice. Strikingly, four weeks of chronic unpredictable stress (CUS) did not further increase passive coping in female astrocytic FAK knockout mice, whereas it exacerbated it in female wildtype mice and male mice of both genotypes. These data suggest that astrocyte FAK inhibition is required for chronic stress-induced passive coping in females. Indeed, CUS reduced phospho-FAK and increased CNTF in the female MeA. Progesterone treatment after ovariectomy activated amygdala FAK and alleviated ovariectomy-induced passive coping in wildtype, but not astrocytic FAK knockout females. This suggests that progesterone-mediated activation of FAK in astrocytes reduces female stress responses. Finally, astrocytic FAK knockout or FAK inhibitor treatment increased CNTF expression in the MeA of both sexes, although not in the hippocampus. As mentioned, MeA CNTF promotes stress responses only in females, which may explain the female-specific role of astrocytic FAK inhibition. Together, this study reveals a novel female-specific progesterone-astrocytic FAK pathway that counteracts CNTF-mediated stress responses and points to opportunities for developing treatments for stress-related disorders in women.

星形胶质细胞与应激反应有关,并能产生睫状神经营养因子(CNTF)。我们在小鼠内侧杏仁核(MeA)中发现,只有雌性星形胶质细胞能促进被动应激反应。药物抑制局灶粘附激酶(FAK)可上调CNTF的表达。在这里,我们发现诱导性敲除星形胶质细胞中的FAK或用FAK抑制剂进行全身治疗可增加雌性小鼠在急性强迫游泳应激试验中的被动应对行为,即不动。令人吃惊的是,四周的慢性不可预测应激(CUS)并没有进一步增加雌性星形胶质细胞FAK基因敲除小鼠的被动应对行为,但却加剧了雌性野生型小鼠和雄性两种基因型小鼠的被动应对行为。这些数据表明,雌性小鼠慢性应激诱导的被动应对需要星形胶质细胞 FAK 抑制。事实上,CUS能减少雌性MeA的磷酸-FAK并增加CNTF。卵巢切除术后的黄体酮治疗激活了杏仁核FAK,缓解了野生型女性卵巢切除术诱导的被动应对,但没有缓解星形胶质细胞FAK基因敲除女性的被动应对。这表明,黄体酮介导的星形胶质细胞 FAK 激活可减轻女性的应激反应。最后,星形胶质细胞FAK敲除或FAK抑制剂处理增加了CNTF在两性MeA中的表达,尽管不是在海马中。如前所述,MeA CNTF只促进女性的应激反应,这可能解释了星形胶质细胞FAK抑制剂的女性特异性作用。总之,这项研究揭示了一种新的女性特异性黄体酮-星形胶质细胞FAK通路,它能抵消CNTF介导的应激反应,并为开发治疗女性应激相关疾病的方法提供了机会。
{"title":"Astrocyte focal adhesion kinase reduces passive stress coping by inhibiting ciliary neurotrophic factor only in female mice","authors":"Cuihong Jia,&nbsp;W. Drew Gill,&nbsp;Chiharu Lovins,&nbsp;Russell W. Brown ,&nbsp;Theo Hagg","doi":"10.1016/j.ynstr.2024.100621","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100621","url":null,"abstract":"<div><p>Astrocytes have been implicated in stress responses and produce ciliary neurotrophic factor (CNTF), which we have shown in the mouse medial amygdala (MeA) to promote passive stress coping response only in females. Pharmacological inhibition of focal adhesion kinase (FAK) upregulates CNTF expression. Here, we found that inducible knockout of FAK in astrocytes or systemic treatment with an FAK inhibitor increased passive coping behavior, i.e., immobility, in an acute forced swim stress test in female, but not male, mice. Strikingly, four weeks of chronic unpredictable stress (CUS) did not further increase passive coping in female astrocytic FAK knockout mice, whereas it exacerbated it in female wildtype mice and male mice of both genotypes. These data suggest that astrocyte FAK inhibition is required for chronic stress-induced passive coping in females. Indeed, CUS reduced phospho-FAK and increased CNTF in the female MeA. Progesterone treatment after ovariectomy activated amygdala FAK and alleviated ovariectomy-induced passive coping in wildtype, but not astrocytic FAK knockout females. This suggests that progesterone-mediated activation of FAK in astrocytes reduces female stress responses. Finally, astrocytic FAK knockout or FAK inhibitor treatment increased CNTF expression in the MeA of both sexes, although not in the hippocampus. As mentioned, MeA CNTF promotes stress responses only in females, which may explain the female-specific role of astrocytic FAK inhibition. Together, this study reveals a novel female-specific progesterone-astrocytic FAK pathway that counteracts CNTF-mediated stress responses and points to opportunities for developing treatments for stress-related disorders in women.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100621"},"PeriodicalIF":5.0,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000171/pdfft?md5=b3c9f46d5085d9d0c7b70b4812056a13&pid=1-s2.0-S2352289524000171-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140134310","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
Environmental enrichment attenuates depressive-like behavior in maternal rats by inhibiting neuroinflammation and apoptosis and promoting neuroplasticity 环境富集通过抑制神经炎症和细胞凋亡以及促进神经可塑性来减轻母鼠的抑郁样行为
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-11 DOI: 10.1016/j.ynstr.2024.100624
Guopeng Chen , Yuhui Zhang , Ruiling Li , Liuyin Jin , Keke Hao , Jingtong Rong , Hao Duan , Yiwei Du , Lihua Yao , Dan Xiang , Zhongchun Liu

Gestational stress can exacerbate postpartum depression (PPD), for which treatment options remain limited. Environmental enrichment (EE) may be a therapeutic intervention for neuropsychiatric disorders, including depression, but the specific mechanisms by which EE might impact PPD remain unknown. Here we examined the behavioral, molecular, and cellular impact of EE in a stable PPD model in rats developed through maternal separation (MS). Maternal rats subjected to MS developed depression-like behavior and cognitive dysfunction together with evidence of significant neuroinflammation including microglia activation, neuronal apoptosis, and impaired synaptic plasticity. Expanding the duration of EE to throughout pregnancy and lactation, we observed an EE-associated reversal of MS-induced depressive phenotypes, inhibition of neuroinflammation and neuronal apoptosis, and improvement in synaptic plasticity in maternal rats. Thus, EE effectively alleviates neuroinflammation, neuronal apoptosis, damage to synaptic plasticity, and consequent depression-like behavior in mother rats experiencing MS-induced PPD, paving the way for new preventive and therapeutic strategies for PPD.

妊娠压力会加重产后抑郁症(PPD),但治疗方法仍然有限。环境富集(EE)可能是治疗包括抑郁症在内的神经精神疾病的一种干预措施,但环境富集可能影响产后抑郁症的具体机制仍不清楚。在这里,我们研究了在通过母鼠分离(MS)建立的稳定 PPD 模型中,EE 对行为、分子和细胞的影响。接受 MS 的母体大鼠会出现抑郁样行为和认知功能障碍,并伴有明显的神经炎症,包括小胶质细胞活化、神经元凋亡和突触可塑性受损。将 EE 的持续时间延长至整个孕期和哺乳期,我们观察到 EE 可逆转 MS 诱导的抑郁表型,抑制神经炎症和神经元凋亡,并改善母体大鼠的突触可塑性。因此,EE能有效缓解神经炎症、神经元凋亡、突触可塑性损伤以及MS诱导的母鼠抑郁样行为,为PPD的预防和治疗新策略铺平道路。
{"title":"Environmental enrichment attenuates depressive-like behavior in maternal rats by inhibiting neuroinflammation and apoptosis and promoting neuroplasticity","authors":"Guopeng Chen ,&nbsp;Yuhui Zhang ,&nbsp;Ruiling Li ,&nbsp;Liuyin Jin ,&nbsp;Keke Hao ,&nbsp;Jingtong Rong ,&nbsp;Hao Duan ,&nbsp;Yiwei Du ,&nbsp;Lihua Yao ,&nbsp;Dan Xiang ,&nbsp;Zhongchun Liu","doi":"10.1016/j.ynstr.2024.100624","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100624","url":null,"abstract":"<div><p>Gestational stress can exacerbate postpartum depression (PPD), for which treatment options remain limited. Environmental enrichment (EE) may be a therapeutic intervention for neuropsychiatric disorders, including depression, but the specific mechanisms by which EE might impact PPD remain unknown. Here we examined the behavioral, molecular, and cellular impact of EE in a stable PPD model in rats developed through maternal separation (MS). Maternal rats subjected to MS developed depression-like behavior and cognitive dysfunction together with evidence of significant neuroinflammation including microglia activation, neuronal apoptosis, and impaired synaptic plasticity. Expanding the duration of EE to throughout pregnancy and lactation, we observed an EE-associated reversal of MS-induced depressive phenotypes, inhibition of neuroinflammation and neuronal apoptosis, and improvement in synaptic plasticity in maternal rats. Thus, EE effectively alleviates neuroinflammation, neuronal apoptosis, damage to synaptic plasticity, and consequent depression-like behavior in mother rats experiencing MS-induced PPD, paving the way for new preventive and therapeutic strategies for PPD.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100624"},"PeriodicalIF":5.0,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000201/pdfft?md5=a7e60b7699895e0d532c22cf951219f7&pid=1-s2.0-S2352289524000201-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140137706","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
The neurocomputational signature of decision-making for unfair offers in females under acute psychological stress 急性心理压力下女性对不公平报价决策的神经计算特征
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-06 DOI: 10.1016/j.ynstr.2024.100622
Guangya Wang , Jun Tang , Zhouqian Yin , Siyu Yu , Xindi Shi , Xiurong Hao , Zhudele Zhao , Yafeng Pan , Shijia Li

Stress is a crucial factor affecting social decision-making. However, its impacts on the behavioral and neural processes of females’ unfairness decision-making remain unclear. Combining computational modeling and functional near-infrared spectroscopy (fNIRS), this study attempted to illuminate the neurocomputational signature of unfairness decision-making in females. We also considered the effect of trait stress coping styles. Forty-four healthy young females (20.98 ± 2.89 years) were randomly assigned to the stress group (n = 21) and the control group (n = 23). Acute psychosocial stress was induced by the Trier Social Stress Test (TSST), and participants then completed the one-shot ultimatum game (UG) as responders. The results showed that acute psychosocial stress reduced the adaptability to fairness and lead to more random decision-making responses. Moreover, in the stress group, a high level of negative coping style predicted more deterministic decision. fNIRS results showed that stress led to an increase of oxy-hemoglobin (HbO) peak in the right temporoparietal junction (rTPJ), while decreased the activation of left middle temporal gyrus (lMTG) when presented the moderately unfair (MU) offers. This signified more involvement of the mentalization and the inhibition of moral processing. Moreover, individuals with higher negative coping scores showed more deterministic decision behaviors under stress. Taken together, our study emphasizes the role of acute psychosocial stress in affecting females’ unfairness decision-making mechanisms in social interactions, and provides evidences for the “tend and befriend” pattern based on a cognitive neuroscience perspec

压力是影响社会决策的一个重要因素。然而,压力对女性不公平决策的行为和神经过程的影响仍不清楚。本研究结合计算建模和功能性近红外光谱(fNIRS),试图揭示女性不公平决策的神经计算特征。我们还考虑了特质压力应对方式的影响。44 名健康的年轻女性(20.98 ± 2.89 岁)被随机分配到压力组(21 人)和对照组(23 人)。通过特里尔社会压力测试(TSST)诱发急性社会心理压力,然后参与者以应答者的身份完成一次性最后通牒游戏(UG)。结果表明,急性社会心理压力降低了参与者对公平的适应性,并导致他们做出更多随机决策反应。fNIRS结果表明,当被试提出中度不公平(MU)的提议时,压力导致右侧颞顶交界处(rTPJ)的氧血红蛋白(HbO)峰值升高,而左侧颞中回(lMTG)的激活程度降低。这表明更多的心智化参与和道德处理的抑制。此外,消极应对得分较高的个体在压力下表现出更多的决定性决策行为。综上所述,我们的研究强调了急性社会心理压力对女性在社会交往中的不公平决策机制的影响,并从认知神经科学的角度为 "倾向和结交 "模式提供了证据。
{"title":"The neurocomputational signature of decision-making for unfair offers in females under acute psychological stress","authors":"Guangya Wang ,&nbsp;Jun Tang ,&nbsp;Zhouqian Yin ,&nbsp;Siyu Yu ,&nbsp;Xindi Shi ,&nbsp;Xiurong Hao ,&nbsp;Zhudele Zhao ,&nbsp;Yafeng Pan ,&nbsp;Shijia Li","doi":"10.1016/j.ynstr.2024.100622","DOIUrl":"10.1016/j.ynstr.2024.100622","url":null,"abstract":"<div><p>Stress is a crucial factor affecting social decision-making. However, its impacts on the behavioral and neural processes of females’ unfairness decision-making remain unclear. Combining computational modeling and functional near-infrared spectroscopy (fNIRS), this study attempted to illuminate the neurocomputational signature of unfairness decision-making in females. We also considered the effect of trait stress coping styles. Forty-four healthy young females (20.98 ± 2.89 years) were randomly assigned to the stress group (<em>n</em> = 21) and the control group (<em>n</em> = 23). Acute psychosocial stress was induced by the Trier Social Stress Test (TSST), and participants then completed the one-shot ultimatum game (UG) as responders. The results showed that acute psychosocial stress reduced the adaptability to fairness and lead to more random decision-making responses. Moreover, in the stress group, a high level of negative coping style predicted more deterministic decision. fNIRS results showed that stress led to an increase of oxy-hemoglobin (HbO) peak in the right temporoparietal junction (rTPJ), while decreased the activation of left middle temporal gyrus (lMTG) when presented the moderately unfair (MU) offers. This signified more involvement of the mentalization and the inhibition of moral processing. Moreover, individuals with higher negative coping scores showed more deterministic decision behaviors under stress. Taken together, our study emphasizes the role of acute psychosocial stress in affecting females’ unfairness decision-making mechanisms in social interactions, and provides evidences for the “tend and befriend” pattern based on a cognitive neuroscience perspec</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100622"},"PeriodicalIF":5.0,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000183/pdfft?md5=ae40407ebdc37063e7971273498b678a&pid=1-s2.0-S2352289524000183-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140092204","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
SNX27: A trans-species cognitive modulator with implications for anxiety and stress susceptibility SNX27:一种跨物种认知调节器,对焦虑和压力易感性有影响
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-03-05 DOI: 10.1016/j.ynstr.2024.100619
Gisela Armada , Susana Roque , Cláudia Serre-Miranda , Liliana Ferreira , Ana Vale , Ana João Rodrigues , Wanjin Hong , Margarida Correia-Neves , Neide Vieira

Sorting Nexin 27 (SNX27) is a brain-enriched endosome-associated cargo adaptor that shapes excitatory control, being relevant for cognitive and reward processing, and for several neurological conditions. Despite this, SNX27's role in the nervous system remains poorly explored. To further understand SNX27 function, we performed an extensive behavioral characterization comprising motor, cognitive and emotional dimensions of SNX27+/− mice. Furthermore, attending on the recently described association between SNX27 function and cellular stress signaling mechanisms in vitro, we explored SNX27-stress interplay using a Caenorhabditis elegans Δsnx-27 mutant and wild-type (WT) rodents after stress exposure.

SNX27+/− mice, as C. elegans Δsnx-27 mutants, present cognitive impairments, highlighting a conserved role for SNX27 in cognitive modulation across species. Interestingly, SNX27 downmodulation leads to anxiety-like behavior in mice evaluated in the Elevated Plus Maze (EPM). This anxious phenotype is associated with increased dendritic complexity of the bed nucleus of the stria terminalis (BNST) neurons, and increased complexity of the basolateral amygdala (BLA) pyramidal neurons. These findings highlight the still unknown role of SNX27 in anxiety regulation.

Moreover, we uncovered a direct link between SNX27 dysfunction and stress susceptibility in C. elegans and found that stress-exposed rodents display decreased SNX27 levels in stress-susceptible brain regions.

Altogether, we provided new insights on SNX27's relevance in anxiety-related behaviors and neuronal structure in stress-associated brain regions.

分选内含蛋白 27(SNX27)是一种脑内富集的内含体相关货物适配体,它能影响兴奋控制,与认知和奖赏处理以及多种神经系统疾病有关。尽管如此,SNX27 在神经系统中的作用仍然鲜为人知。为了进一步了解 SNX27 的功能,我们对 SNX27+/- 小鼠的运动、认知和情绪等方面进行了广泛的行为特征描述。此外,根据最近描述的SNX27功能与体外细胞应激信号转导机制之间的联系,我们利用草履虫Δsnx-27突变体和野生型(WT)啮齿动物在应激暴露后探索了SNX27与应激之间的相互作用。有趣的是,SNX27 下调会导致小鼠在高架迷宫(EPM)中出现类似焦虑的行为。这种焦虑表型与纹状体末端床核(BNST)神经元树突复杂性的增加以及杏仁基底外侧(BLA)锥体神经元复杂性的增加有关。这些发现突显了SNX27在焦虑调控中仍未知的作用。此外,我们还发现了SNX27功能障碍与优雅鼠的应激易感性之间的直接联系,并发现应激暴露的啮齿类动物在应激易感脑区的SNX27水平降低。
{"title":"SNX27: A trans-species cognitive modulator with implications for anxiety and stress susceptibility","authors":"Gisela Armada ,&nbsp;Susana Roque ,&nbsp;Cláudia Serre-Miranda ,&nbsp;Liliana Ferreira ,&nbsp;Ana Vale ,&nbsp;Ana João Rodrigues ,&nbsp;Wanjin Hong ,&nbsp;Margarida Correia-Neves ,&nbsp;Neide Vieira","doi":"10.1016/j.ynstr.2024.100619","DOIUrl":"10.1016/j.ynstr.2024.100619","url":null,"abstract":"<div><p>Sorting Nexin 27 (SNX27) is a brain-enriched endosome-associated cargo adaptor that shapes excitatory control, being relevant for cognitive and reward processing, and for several neurological conditions. Despite this, SNX27's role in the nervous system remains poorly explored. To further understand SNX27 function, we performed an extensive behavioral characterization comprising motor, cognitive and emotional dimensions of SNX27<sup>+/−</sup> mice. Furthermore, attending on the recently described association between SNX27 function and cellular stress signaling mechanisms <em>in vitro</em>, we explored SNX27-stress interplay using a <em>Caenorhabditis elegans Δsnx-27</em> mutant and wild-type (WT) rodents after stress exposure.</p><p>SNX27<sup>+/−</sup> mice, as <em>C. elegans Δsnx-27</em> mutants, present cognitive impairments, highlighting a conserved role for SNX27 in cognitive modulation across species. Interestingly, SNX27 downmodulation leads to anxiety-like behavior in mice evaluated in the Elevated Plus Maze (EPM). This anxious phenotype is associated with increased dendritic complexity of the bed nucleus of the stria terminalis (BNST) neurons, and increased complexity of the basolateral amygdala (BLA) pyramidal neurons. These findings highlight the still unknown role of SNX27 in anxiety regulation.</p><p>Moreover, we uncovered a direct link between SNX27 dysfunction and stress susceptibility in <em>C. elegans</em> and found that stress-exposed rodents display decreased SNX27 levels in stress-susceptible brain regions.</p><p>Altogether, we provided new insights on SNX27's relevance in anxiety-related behaviors and neuronal structure in stress-associated brain regions.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"30 ","pages":"Article 100619"},"PeriodicalIF":5.0,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000158/pdfft?md5=80925083eafe26aeb3cf8789dfbb0c8d&pid=1-s2.0-S2352289524000158-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140092692","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
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.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1