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Prior experience with behavioral control over stress facilitates social dominance 先前的压力行为控制经验有助于社会支配
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-12-06 DOI: 10.1016/j.ynstr.2023.100597
Philip T. Coleman , Gabriel W. Costanza-Chavez , Heather N. Martin, Jose Amat, Matthew G. Frank, Rory J. Sanchez, Garrett J. Potter, Simone M. Mellert, Rene K. Carter, Gianni N. Bonnici, Steven F. Maier, Michael V. Baratta

Dominance status has extensive effects on physical and mental health, and an individual's relative position can be shaped by experiential factors. A variety of considerations suggest that the experience of behavioral control over stressors should produce winning in dominance tests and that winning should blunt the impact of later stressors, as does prior control. To investigate the interplay between competitive success and stressor control, we first examined the impact of stressor controllability on subsequent performance in a warm spot competition test modified for rats. Prior experience of controllable, but not physically identical uncontrollable, stress increased later effortful behavior and occupation of the warm spot. Controllable stress subjects consistently ranked higher than did uncontrollable stress subjects. Pharmacological inactivation of the prelimbic (PL) cortex during behavioral control prevented later facilitation of dominance. Next, we explored whether repeated winning experiences produced later resistance against the typical sequelae of uncontrollable stress. To establish dominance status, triads of rats were given five sessions of warm spot competition. The development of stable dominance was prevented by reversible inactivation of the PL or NMDA receptor blockade in the dorsomedial striatum. Stable winning blunted the later stress-induced increase in dorsal raphe nucleus serotonergic activity, as well as prevented uncontrollable stress-induced social avoidance. In contrast, endocrine and neuroimmune responses to uncontrollable stress were unaffected, indicating a selective impact of prior dominance. Together, these data demonstrate that instrumental control over stress promotes later dominance, but also reveal that winning experiences buffer against the neural and behavioral outcomes of future adversity.

支配地位对身心健康有广泛的影响,个体的相对地位可由经验因素塑造。各种各样的考虑表明,对压力源的行为控制的经验应该产生优势测试的胜利,并且胜利应该减弱后压力源的影响,就像先前的控制一样。为了研究竞争成功与压力源控制之间的相互作用,我们首先在一个改良的大鼠温点竞争测试中研究了压力源可控性对随后表现的影响。先前的可控经验,但不是物理上相同的不可控,压力增加了后来的努力行为和占领温暖点。可控压力组的排名始终高于不可控压力组。在行为控制期间,前边缘(PL)皮层的药理学失活阻止了后来的优势化。接下来,我们探讨了重复的胜利经历是否会产生后来对不可控制的压力的典型后遗症的抵抗力。为了建立优势地位,给三联大鼠进行5次温点竞争。背内侧纹状体中PL或NMDA受体阻断的可逆失活阻止了稳定优势的发展。稳定的胜利减弱了后期压力引起的中缝背核血清素活性的增加,并阻止了无法控制的压力引起的社会回避。相比之下,内分泌和神经免疫对不可控压力的反应不受影响,表明先前优势的选择性影响。总之,这些数据表明,对压力的工具控制促进了后来的支配地位,但也揭示了胜利的经历缓冲了未来逆境的神经和行为结果。
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引用次数: 0
Glucocorticoids modulate neural activity via a rapid non-genomic effect on Kv2.2 channels in the central nervous system 糖皮质激素通过对中枢神经系统Kv2.2通道的快速非基因组效应调节神经活动
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-25 DOI: 10.1016/j.ynstr.2023.100593
Yuqi Wang , Yuchen Zhang , Jiawei Hu , Chengfang Pan , Yiming Gao , Qingzhuo Liu , Wendong Xu , Lei Xue , Changlong Hu

Glucocorticoids are primary stress hormones that exert neuronal effects via both genomic and non-genomic signaling pathways. However, their rapid non-genomic effects and underlying mechanisms on neural activities remain elusive. In the present study, we investigated the rapid non-genomic effect of glucocorticoids on Kv2.2 channels in cultured HEK293 cells and acute brain slices including cortical pyramidal neurons and calyx-type synapses in the brain stem. We found that cortisol, the endogenous glucocorticoids, rapidly increased Kv2.2 currents by increasing the single-channel open probability in Kv2.2-expressing HEK293 cells through activation of the membrane-associated glucocorticoid receptor. Bovine serum albumin-conjugated dexamethasone, a membrane-impermeable agonist of the glucocorticoid receptor, could mimic the effect of cortisol on Kv2.2 channels. The cortisol-increased Kv2.2 currents were induced by activation of the extracellular signal-regulated protein kinase (ERK) 1/2 kinase, which could be inhibited by U0126, an antagonist of the ERK signaling pathway. In layer 2 cortical pyramidal neurons and the calyx of Held synapses, cortisol suppressed the action potential firing frequency during depolarization and reduced the successful rate upon high-frequency stimulation by activating Kv2.2 channels. We further examined the postsynaptic responses and found that cortisol did not affect the mEPSC and evoked EPSC, but increased the activity-dependent synaptic depression induced by a high-frequency stimulus train. In conclusion, glucocorticoids can rapidly activate Kv2.2 channels through membrane-associated glucocorticoid receptors via the ERK1/2 signaling pathway, suppress presynaptic action potential firing, and inhibit synaptic transmission and plasticity. This may be a universal mechanism of the glucocorticoid-induced non-genomic effects in the central nervous system.

糖皮质激素是主要的应激激素,通过基因组和非基因组信号通路发挥神经元作用。然而,它们对神经活动的快速非基因组效应和潜在机制仍然难以捉摸。在本研究中,我们研究了糖皮质激素对培养的HEK293细胞和包括皮质锥体神经元和脑干花萼型突触在内的急性脑切片中Kv2.2通道的快速非基因组效应。我们发现,内源性糖皮质激素皮质醇通过激活膜相关糖皮质激素受体,增加表达Kv2.2的HEK293细胞的单通道打开概率,从而迅速增加Kv2.2电流。牛血清白蛋白偶联地塞米松是一种糖皮质激素受体的膜不渗透性激动剂,可以模拟皮质醇对Kv2.2通道的作用。皮质醇增加的Kv2.2电流是通过激活细胞外信号调节蛋白激酶(ERK) 1/2激酶诱导的,该激酶可被ERK信号通路拮抗剂U0126抑制。在皮层第2层锥体神经元和Held突触的花萼中,皮质醇通过激活Kv2.2通道抑制去极化过程中的动作电位放电频率,降低高频刺激的成功率。我们进一步检查了突触后反应,发现皮质醇不影响mEPSC并诱发EPSC,但增加了高频刺激引起的活动依赖性突触抑制。综上所述,糖皮质激素可通过膜相关糖皮质激素受体通过ERK1/2信号通路快速激活Kv2.2通道,抑制突触前动作电位放电,抑制突触传递和可塑性。这可能是糖皮质激素诱导中枢神经系统非基因组效应的普遍机制。
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引用次数: 0
Environmental enrichment reverses stress-induced changes in the brain-gut axis to ameliorate chronic visceral and somatic hypersensitivity 环境富集逆转应激诱导的脑肠轴变化,改善慢性内脏和躯体超敏反应
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-24 DOI: 10.1016/j.ynstr.2023.100590
A. Orock , A.C. Johnson , E. Mohammadi , B. Greenwood-Van Meerveld

Introduction

Behavioral therapies, including cognitive behavioral therapy, hypnotherapy and stress management activities, have emerged as effective treatments for irritable bowel syndrome (IBS), a female predominant disorder of the brain-gut axis. IBS, affecting over 10% of the global population, typically presents with abnormal bowel habits and abdominal pain due to visceral hypersensitivity. While the mechanisms underlying how behavioral therapies treat IBS are still elusive, we had previously shown that chronic stress alters gene expression in brain regions critical for stress processing and nociception. We found that exposure to an enriched environment (EE), the rodent analogue of behavioral therapies, prior to and during the stressor was sufficient to prevent stress-induced changes in glucocorticoid receptor (GR) expression in the central nucleus of the amygdala (CeA) and hippocampus. Pre-exposure to EE also inhibited stress-induced increased colonic permeability and was able to block the induction of stress-induced visceral and somatic hypersensitivity. However, it remains unknown if EE can reverse chronic viscerosomatic hypersensitivity that persists following exposure to stress. We hypothesized that EE after chronic stress would be sufficient to reverse stress-induced changes in i) GR expression in the CeA and hippocampus, ii) ameliorate stress-induced colonic hyperpermeability and iii) restore normal visceral and somatic sensitivity in male and female rats.

Methods

Male and female rats were exposed to daily water avoidance stress (WAS). After confirming the rats had developed visceral hypersensitivity, 50% of the animals were housed in EE for 2 weeks while the other 50% remained in standard housing (SH). At the end of this period, we assessed visceral and somatic sensitivity. We also collected colon tissue to measure colonic permeability. Micro-punches of tissue from the CeA and hippocampus were isolated to measure GR expression. Control animals not exposed to WAS were kept in SH for the duration of the study (n = 8 per group).

Results

In both male and female rats, EE reversed stress-induced visceral (p < 0.001) and somatic (p < 0.01) hypersensitivity when compared to WAS animals housed in SH to levels comparable to control animals. EE exposure also reversed changes in GR expression in both the hippocampus (p < 0.01) and CeA (p < 0.01), normalizing GR expression to control levels. EE exposure ameliorated stress-induced colonic hyperpermeability in both male (p < 0.01) and female (p < 0.01) rats compared to WAS rats in SH.

Conclusion

Our findings suggest that behavioral therapies are viable therapeutic options for IBS as they can counter the stress-induced pathophysiology underlying IBS symptoms including visceral hypersensitivity, increased colonic permeability and altered gene expression.

行为疗法,包括认知行为疗法、催眠疗法和压力管理活动,已经成为肠易激综合征(IBS)的有效治疗方法,IBS是一种女性主要的脑-肠轴疾病。IBS影响全球10%以上的人口,通常表现为肠道习惯异常和内脏过敏引起的腹痛。虽然行为疗法治疗肠易激综合征的机制仍然难以捉摸,但我们之前已经表明,慢性压力会改变大脑中对压力处理和伤害感觉至关重要的区域的基因表达。我们发现,在应激源之前和期间暴露于富集环境(EE),即行为治疗的啮齿动物模拟物,足以防止应激引起的杏仁核中央核(CeA)和海马糖皮质激素受体(GR)表达的变化。预暴露于EE也抑制应激诱导的结肠通透性增加,并能够阻断应激诱导的内脏和躯体超敏反应的诱导。然而,EE是否可以逆转暴露于压力后持续存在的慢性脏器体超敏反应仍不清楚。我们假设慢性应激后的EE足以逆转应激诱导的变化:1)CeA和海马GR表达,2)改善应激诱导的结肠高通透性,3)恢复雄性和雌性大鼠正常的内脏和身体敏感性。方法将雄性和雌性大鼠置于每日避水应激(WAS)下。在确认大鼠出现内脏过敏后,50%的动物被安置在EE中2周,而另外50%的动物仍被安置在标准住房(SH)中。在这一阶段结束时,我们评估了内脏和躯体的敏感性。我们还收集结肠组织测量结肠通透性。从CeA和海马组织中分离微孔,测定GR表达。未暴露于WAS的对照动物在研究期间保持在SH中(每组n = 8)。结果在雄性和雌性大鼠中,EE均能逆转应激诱导的内脏(p <0.001)和躯体(p <0.01),与被置于SH环境中的WAS动物相比,过敏程度与对照动物相当。EE暴露也逆转了海马中GR表达的变化(p <0.01)和CeA (p <0.01),使GR表达正常化至控制水平。EE暴露可改善应激性结肠高通透性(p <0.01)和女性(p <结论我们的研究结果表明,行为疗法是治疗IBS的可行选择,因为它们可以对抗应激诱导的IBS症状的病理生理,包括内脏过敏、结肠通透性增加和基因表达改变。
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引用次数: 0
Microglia are necessary for probiotics supplementation to improve impaired fear extinction caused by pregnancy stress in adult offspring of rats 小胶质细胞是补充益生菌改善大鼠成年后代妊娠应激引起的恐惧消退障碍所必需的
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-19 DOI: 10.1016/j.ynstr.2023.100591
Ru Zeng , Jie Chen , Yihan Peng , Weiye Xu , Yuanyuan Tao , Min Li , Ruqi Zhang , Jingzhuo Meng , Zhiyuan Li , Leping Zeng , Jufang Huang

The prevention and treatment of fear-related disorders in offspring affected by pregnancy stress remains challenging at clinic. Here, we examined the effects of gut microbiota of stressed pregnant rats on the fear extinction of their offsprings, and the potential mechanisms. We found that gut microbiota transplantation from rats with pregnancy stress to normal pregnant rats impaired fear extinction, induced microglial activation and synaptic phagocytosis, increased synapse loss in offsprings. Probiotics supplement during pregnancy stress partly normalized pregnancy stress-induced gut microbiota dysbiosis of pregnant rats, and promoted fear memory extinction, inhibited fear memory reappearance, and limited microglial activation and synaptic phagocytosis in offsprings. These data revealed that gut microbiota of stressed pregnant mother improved the development of fear-related disorders of offspring, which may be associated with microglial synaptic pruning.

预防和治疗受妊娠压力影响的后代的恐惧相关障碍在临床上仍然具有挑战性。在这里,我们研究了应激怀孕大鼠肠道微生物群对其后代恐惧灭绝的影响及其潜在机制。我们发现,将妊娠应激大鼠的肠道菌群移植到正常妊娠大鼠的后代中,会损害恐惧消退,诱导小胶质细胞激活和突触吞噬,增加突触损失。妊娠应激期间补充益生菌可部分缓解妊娠应激引起的妊娠大鼠肠道菌群失调,促进后代恐惧记忆消退,抑制恐惧记忆重现,限制小胶质细胞激活和突触吞噬。这些数据表明,压力孕妇的肠道微生物群改善了后代恐惧相关疾病的发展,这可能与小胶质突触修剪有关。
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引用次数: 0
Association between gut microbiota and its functional metabolites with prenatal depression in women 肠道菌群及其功能代谢物与妇女产前抑郁症的关系
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-17 DOI: 10.1016/j.ynstr.2023.100592
Tianqu Xie , Xiaoxiao Fan , Hanghang Pang , Tianzi Zang , Ni Wu , Juan Liu , Ziying Li , Sha Li , Quanfei Zhu , Julia Elise Slack , Jinbing Bai , Yu Xu , Yanqun Liu

Background

The gut microbiota may affect mood through the microbiota-gut-brain axis. The purpose of this study was to examine the effect of the gut microbiota and its metabolites, such as short-chain fatty acids (SCFAs), on prenatal depression and to determine the role of 5-hydroxytryptamine (5-HT) on prenatal depression in association with the gut microbiota and its metabolites (i.e. SCFAs).

Methods

Eighty-six pregnant women in the third trimester were recruited. Prenatal depression was determined by a score of 10 via the Edinburgh Postpartum Depression Scale. Demographic data, stool, and blood samples were collected. The gut microbiota and its metabolites SCFAs were determined by 16S rRNA gene sequencing and liquid chromatography-mass spectrometry analysis. Plasma 5-HT was determined by gas chromatography-mass spectrometry analysis.

Results

After controlling relevant covariates, our results found the higher the abundance of Candidatus_Soleaferrea, the lower the risk of prenatal depression; the higher the concentration of propanoic acid, the higher risk of prenatal depression. Our results also found the lower the plasma 5-HT, the higher the risk of prenatal depression, and 5-HT was related to unclassified_c_Clostridia and NK4A214_group. However, results of this study did not support the moderating effect of plasma 5-HT on the association of Candidatus_Soleaferrea or propionic acid with prenatal depression.

Conclusions

Results of this study supported that changes in certain gut microbiota, SCFAs, and plasma 5-HT during pregnancy were associated with prenatal depression. This finding provides new ideas for interventions based on diet or probiotics to regulate mood during pregnancy.

肠道菌群可能通过菌群-肠-脑轴影响情绪。本研究的目的是研究肠道微生物群及其代谢物,如短链脂肪酸(SCFAs)对产前抑郁症的影响,并确定5-羟色胺(5-HT)在与肠道微生物群及其代谢物(即SCFAs)相关的产前抑郁症中的作用。方法选取孕晚期孕妇86例。产前抑郁是通过爱丁堡产后抑郁量表以10分来确定的。收集了人口统计资料、粪便和血液样本。采用16S rRNA基因测序和液相色谱-质谱分析方法测定肠道菌群及其代谢产物SCFAs。采用气相色谱-质谱法测定血浆5-羟色胺含量。结果在控制相关变量后发现,Candidatus_Soleaferrea丰度越高,产前抑郁风险越低;丙酸浓度越高,产前抑郁的风险越高。我们的研究结果还发现,血浆5-HT越低,产前抑郁的风险越高,5-HT与unclassified_c_Clostridia和NK4A214_group有关。然而,本研究结果不支持血浆5-羟色胺在Candidatus_Soleaferrea或丙酸与产前抑郁的关联中的调节作用。结论妊娠期某些肠道菌群、scfa和血浆5-羟色胺的变化与产前抑郁有关。这一发现为基于饮食或益生菌的干预来调节怀孕期间的情绪提供了新的思路。
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引用次数: 0
Imbalanced glucocorticoid and mineralocorticoid stress hormone receptor function has sex-dependent and independent regulatory effects in the mouse hippocampus 糖皮质激素和矿皮质激素应激激素受体功能失衡在小鼠海马中具有性别依赖和独立的调节作用
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-17 DOI: 10.1016/j.ynstr.2023.100589
Robert H. Oakley , Natallia V. Riddick , Sheryl S. Moy , John A. Cidlowski

Many stress-related neuropsychiatric disorders display pronounced sex differences in their frequency and clinical symptoms. Glucocorticoids are primary stress hormones that have been implicated in the development of these disorders but whether they contribute to the observed sex bias is poorly understood. Glucocorticoids signal through two closely related nuclear receptors, the glucocorticoid (GR) and mineralocorticoid receptor (MR). To elucidate the sex-specific and independent actions of glucocorticoids in the hippocampus, we developed knockout mice lacking hippocampal GR, MR, or both GR and MR. Mice deficient in hippocampal MR or both GR and MR showed an altered molecular phenotype of CA2 neurons and reduced anxiety-like behavior in both sexes, but altered stress adaptation behavior only in females and enhanced fear-motivated cue learning only in males. All three knockout mouse models displayed reduced sociability but only in male mice. Male and female mice deficient in both hippocampal GR and MR exhibited extensive neurodegeneration in the dentate gyrus. Global transcriptomic analysis revealed a marked expansion in the number of dysregulated genes in the hippocampus of female knockout mice compared to their male counterparts; however, the overall patterns of gene dysregulation were remarkably similar in both sexes. Within and across sex comparisons identified key GR and MR target genes and associated signaling pathways underlying the knockout phenotypes. These findings define major sex-dependent and independent effects of GR/MR imbalances on gene expression and functional profiles in the hippocampus and inform new strategies for treating men and women with stress-related neuropsychiatric disorders.

许多与压力相关的神经精神疾病在发病频率和临床症状上表现出明显的性别差异。糖皮质激素是主要的应激激素,与这些疾病的发展有关,但它们是否有助于观察到的性别偏见尚不清楚。糖皮质激素通过两个密切相关的核受体糖皮质激素(GR)和矿皮质激素受体(MR)发出信号。为了阐明糖皮质激素在海马体中的性别特异性和独立作用,我们开发了缺乏海马GR、MR或同时缺乏GR和MR的敲除小鼠,海马MR或同时缺乏GR和MR的小鼠在两性中都表现出CA2神经元分子表型的改变和焦虑样行为的减少,但仅在雌性中改变了应激适应行为,仅在雄性中增强了恐惧动机线索学习。所有三种基因敲除小鼠模型都表现出社交能力下降,但仅在雄性小鼠中。海马GR和MR均缺乏的雄性和雌性小鼠在齿状回表现出广泛的神经变性。全球转录组学分析显示,与雄性敲除小鼠相比,雌性敲除小鼠海马中失调基因的数量显着增加;然而,基因失调的总体模式在两性中是非常相似的。性别内部和跨性别比较确定了关键的GR和MR靶基因以及敲除表型的相关信号通路。这些发现确定了GR/MR失衡对海马体基因表达和功能谱的主要性别依赖和独立影响,并为治疗男性和女性压力相关神经精神疾病提供了新的策略。
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引用次数: 0
The importance of REM sleep fragmentation in the effects of stress on sleep: Perspectives from preclinical studies 快速眼动睡眠片段在压力对睡眠影响中的重要性:来自临床前研究的观点
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-14 DOI: 10.1016/j.ynstr.2023.100588
Laura Grafe , Katherine E. Miller , Richard J. Ross , Seema Bhatnagar

Psychological stress poses a risk for sleep disturbances. Importantly, trauma-exposed individuals who develop posttraumatic stress disorder (PTSD) frequently report insomnia and recurrent nightmares. Clinical studies have provided insight into the mechanisms of these sleep disturbances. We review polysomnographic findings in PTSD and identify analogous measures that have been made in animal models of PTSD. There is a rich empirical and theoretical literature on rapid eye movement sleep (REMS) substrates of insomnia and nightmares, with an emphasis on REMS fragmentation. For future investigations of stress-induced sleep changes, we recommend a focus on tonic, phasic and other microarchitectural REMS measures. Power spectral density analysis of the sleep EEG should also be utilized. Animal models with high construct validity can provide insight into gender and time following stressor exposure as moderating variables. Ultimately, preclinical studies with translational potential will lead to improved treatment for stress-related sleep disturbances.

心理压力会造成睡眠障碍。重要的是,创伤暴露的个体发展为创伤后应激障碍(PTSD)经常报告失眠和反复的噩梦。临床研究已经对这些睡眠障碍的机制提供了深入的了解。我们回顾了创伤后应激障碍的多导睡眠图发现,并确定了在创伤后应激障碍动物模型中所做的类似措施。关于快速眼动睡眠(REMS)对失眠和噩梦的影响,已有丰富的实证和理论文献,重点是REMS碎片化。对于未来压力诱发睡眠变化的研究,我们建议将重点放在紧张性、相位性和其他微结构性REMS测量上。还应利用睡眠脑电图的功率谱密度分析。具有高结构效度的动物模型可以提供性别和压力暴露时间作为调节变量的洞见。最终,具有转化潜力的临床前研究将改善与压力相关的睡眠障碍的治疗。
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引用次数: 0
Genomic glucocorticoid receptor effects guide acute stress-induced delayed anxiety and basolateral amygdala spine plasticity in rats 基因组糖皮质激素受体影响大鼠急性应激诱导的延迟性焦虑和杏仁核基底外侧脊柱可塑性
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-10 DOI: 10.1016/j.ynstr.2023.100587
Leonardo S. Novaes , Leticia M. Bueno-de-Camargo , Amadeu Shigeo-de-Almeida , Vitor A.L. Juliano , Ki Goosens , Carolina D. Munhoz

Anxiety, a state related to anticipatory fear, can be adaptive in the face of environmental threats or stressors. However, anxiety can also become persistent and manifest as anxiety- and stress-related disorders, such as generalized anxiety or post-traumatic stress disorder (PTSD). In rodents, systemic administration of glucocorticoids (GCs) or short-term restraint stress induces anxiety-like behaviors and dendritic branching within the basolateral complex of the amygdala (BLA) ten days later. Additionally, increased arousal-related memory retention mediated by elevated GCs requires concomitant noradrenaline (NE) signaling, both acting in the BLA. It is unknown whether GCs and NE play a role in the delayed acute stress-induced effects on behavior and BLA dendritic plasticity. Here, inhibiting corticosterone (CORT) elevation during 2 h of restraint stress prevents stress-induced increases in delayed anxiety-like behavior and BLA dendritic spine density in rats. Also, we show that the delayed acute stress-induced effects on behavior and morphological alterations are critically dependent on genomic glucocorticoid receptor (GR) actions in the BLA. Unlike CORT, the pharmacological enhancement of NE signaling in the BLA was insufficient to drive delayed anxiety-related behavior. Nonetheless, the delayed anxiety-like behavior ten days after acute stress requires NE signaling in the BLA during stress exposure. Therefore, we define the essential roles of two stress-related hormones for the late stress consequences, acting at two separate times: CORT, via GR, immediately during stress, and NE, via beta-adrenoceptors, during the expression of delayed anxiety.

焦虑是一种与预期恐惧相关的状态,在面对环境威胁或压力源时可以适应。然而,焦虑也可能持续存在,表现为焦虑和压力相关的疾病,如广泛性焦虑或创伤后应激障碍(PTSD)。在啮齿类动物中,全身给予糖皮质激素(GCs)或短期约束应激可在10天后诱导杏仁核基底外侧复合体(BLA)内的焦虑样行为和树突分支。此外,由GCs升高介导的觉醒相关记忆保留的增加需要伴随去甲肾上腺素(NE)信号,两者都在BLA中起作用。目前尚不清楚GCs和NE是否在延迟急性应力诱导的行为和BLA树突可塑性的影响中发挥作用。在本研究中,抑制抑制应激2小时时皮质酮(CORT)升高可防止应激诱导的延迟性焦虑样行为和大鼠BLA树突棘密度的增加。此外,我们还表明,延迟急性应激诱导的行为和形态改变的影响严重依赖于BLA中基因组糖皮质激素受体(GR)的作用。与CORT不同,BLA中NE信号的药理增强不足以驱动延迟的焦虑相关行为。然而,急性应激后10天的延迟焦虑样行为需要应激暴露期间BLA中的NE信号。因此,我们确定了两种与压力相关的激素在后期压力后果中的重要作用,它们在两个不同的时间起作用:CORT,通过GR,在压力期间立即起作用,NE,通过β -肾上腺素受体,在延迟焦虑的表达期间起作用。
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引用次数: 0
Estimating foraging behavior in rodents using a modified paradigm measuring threat imminence dynamics 用一种改进的测量威胁迫近动态的范式估计啮齿动物的觅食行为
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-07 DOI: 10.1016/j.ynstr.2023.100585
Xianzong Meng , Ping Chen , Andor Veltien , Tony Palavra , Sjors In't Veld , Joanes Grandjean , Judith R. Homberg

Animals need to respond to threats to avoid danger and approach rewards. In nature, these responses did not evolve alone but are always accompanied by motivational conflict. A semi-naturalistic threat imminence continuum model models the approach-avoidance conflict and is able to integrate multiple behaviors into a single paradigm. However, its comprehensive application is hampered by the lack of a detailed protocol and data about some fundamental factors including sex, age, and motivational level. Here, we modified a previously established paradigm measuring threat imminence continuum dynamics, involving modifications of training and testing protocols, and utilization of commercial materials combined with open science codes, making it easier to replicate. We demonstrate that foraging behavior is modulated by age, hunger level, and sex. This paradigm can be used to study foraging behaviors in animals in a more naturalistic manner with relevance to human approach-avoid conflicts and associated psychopathologies.

动物需要对威胁做出反应以避免危险并接近奖励。在自然界中,这些反应并不是单独进化的,而是总是伴随着动机冲突。一个半自然的威胁迫在眉睫的连续体模型对方法回避冲突进行建模,并能够将多种行为整合到一个单一的范式中。然而,由于缺乏关于性别、年龄和动机水平等一些基本因素的详细方案和数据,它的全面应用受到了阻碍。在这里,我们修改了之前建立的衡量威胁紧迫性连续动力学的范式,包括修改训练和测试协议,以及利用商业材料与开放科学代码相结合,使其更容易复制。我们证明,觅食行为受年龄、饥饿程度和性别的调节。该范式可用于以更自然的方式研究动物的觅食行为,并与人类避免冲突和相关精神病理学的方法相关。
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引用次数: 0
Cortical volume alteration in the superior parietal region mediates the relationship between childhood abuse and PTSD avoidance symptoms: A complementary multimodal neuroimaging study 上顶叶皮质体积改变介导童年虐待与PTSD回避症状之间的关系:一项互补的多模态神经影像学研究
IF 5 2区 医学 Q1 NEUROSCIENCES Pub Date : 2023-11-07 DOI: 10.1016/j.ynstr.2023.100586
Richard Okyere Nkrumah , Claudius von Schröder , Traute Demirakca , Christian Schmahl , Gabriele Ende

Background

Adverse childhood experiences (ACE), which can be separated into abuse and neglect, contribute to the development of post-traumatic stress symptoms (PTSS). However, which brain structures are mainly affected by ACE as well as the mediating role these brain structures play in ACE and PTSS relationship are still being investigated. The current study tested the effect of ACE on brain structure and investigated the latter's mediating role in ACE-PTSS relationship.

Methods

A total of 78 adults with self-reported ACE were included in this study. Participants completed the childhood trauma questionnaire (CTQ) and a Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5) to ascertain ACE history and PTSS, respectively. T1w images and diffusion MRI scans were then acquired to assess cortical morphometry and white matter (WM) integrity in fibre tracts connecting key areas where ACE-related cortical volume alterations were observed.

Results

The combined effect of ACE was negatively associated with total grey matter volume and local cortical area in the right superior parietal region (rSP). Childhood abuse was negatively related to right superior parietal volume after controlling for neglect and overall psychological burden. The right superior parietal volume significantly mediated the relationship between childhood abuse and avoidance-related PTSS. Post-hoc analyses showed that the indirect relation was subsequently moderated by dissociative symptoms. Lastly, a complementary examination of the WM tracts connected to abuse-associated cortical GM regions shows that abuse was negatively related to the normalised fibre density of WM tracts connected to the right superior parietal region.

Conclusion

We provide multimodal structural evidence that ACE in the first years of life is related to alterations in the right superior brain region, which plays a crucial role in spatial processing and attentional functioning. Additionally, we highlight that the cortical volume alteration in this region may play a role in explaining the relationship between childhood abuse and avoidance symptoms.

不良的童年经历(ACE)可分为虐待和忽视,有助于创伤后应激症状(PTSS)的发展。然而,ACE主要影响哪些脑结构以及这些脑结构在ACE与ptsd关系中的中介作用仍在研究中。本研究检验ACE对脑结构的影响,并探讨后者在ACE- ptss关系中的中介作用。方法本研究共纳入78例自报ACE的成人。参与者分别完成童年创伤问卷(CTQ)和创伤后应激障碍检查表(PCL-5)以确定ACE病史和创伤后应激障碍。然后获得T1w图像和弥散MRI扫描,以评估连接关键区域的纤维束的皮层形态测量和白质(WM)完整性,在这些区域观察到与ace相关的皮质体积改变。结果ACE的联合作用与脑灰质总量和右侧顶叶上区局部皮质面积呈负相关。在控制忽视和整体心理负担后,儿童虐待与右顶叶上容积呈负相关。右顶叶上容积显著调节儿童虐待与回避相关性ptsd之间的关系。事后分析表明,这种间接关系随后被分离症状所缓和。最后,对与虐待相关的皮质GM区域相连的WM束的补充检查表明,虐待与与右顶叶上区相连的WM束的正常化纤维密度呈负相关。结论我们提供的多模态结构证据表明,1岁时ACE与右脑上区改变有关,右脑上区在空间加工和注意功能中起着至关重要的作用。此外,我们强调该区域的皮质体积改变可能在解释儿童虐待和回避症状之间的关系中起作用。
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引用次数: 0
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Neurobiology of Stress
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