Neurobiology of Stress最新文献

{"title":"Acute stress yields a sex-dependent facilitation of signaled active avoidance in rats","authors":"Samantha L. Plas ,&nbsp;Cecily R. Oleksiak ,&nbsp;Claire Pitre ,&nbsp;Chance Melton ,&nbsp;Justin M. Moscarello ,&nbsp;Stephen Maren","doi":"10.1016/j.ynstr.2024.100656","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100656","url":null,"abstract":"<div><p>Post-traumatic stress disorder (PTSD) is a debilitating disorder characterized by excessive fear, hypervigilance, and avoidance of thoughts, situations or reminders of the trauma. Among these symptoms, relatively little is known about the etiology of pathological avoidance. Here we sought to determine whether acute stress influences avoidant behavior in adult male and female rats. We used a stress procedure (unsignaled footshock) that is known to induce long-term sensitization of fear and potentiate aversive learning. Rats were submitted to the stress procedure and, one week later, underwent two-way signaled active avoidance conditioning (SAA). In this task, rats learn to prevent an aversive outcome (shock) by performing a shuttling response when exposed to a warning signal (tone). We found that acute stress significantly enhanced SAA acquisition rate in females, but not males. Female rats exhibited significantly greater avoidance responding on the first day of training relative to controls, reaching similar levels of performance by the second day. Males that underwent the stress procedure showed similar rates of acquisition to controls but exhibited resistance to extinction. This was manifest as both elevated avoidance and intertrial responding across extinction days relative to non-stressed controls, an effect that was not observed in females. In a second experiment, acute stress sensitized footshock unconditioned responses in males, not females. However, males and females exhibited similar levels of stress-enhanced fear learning (SEFL), which was expressed as sensitized freezing to a shock-paired context. Together, these results reveal that acute stress facilitates SAA performance in both male and female rats, though the nature of this effect is different in the two sexes. We did not observe sex differences in SEFL, suggesting that the stress-induced sex difference in performance was selective for instrumental avoidance. Future work will elucidate the neurobiological mechanisms underlying the differential effect of stress on instrumental avoidance in male and female rats.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100656"},"PeriodicalIF":5.0,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000523/pdfft?md5=783b8d2f46ff94903921f0240c91287e&pid=1-s2.0-S2352289524000523-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141424532","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}

{"title":"No effects of acute stress on monetary delay discounting: A systematic literature review and meta-analysis","authors":"Paul A.G. Forbes ,&nbsp;Jonas P. Nitschke ,&nbsp;Nicole Hochmeister ,&nbsp;Tobias Kalenscher ,&nbsp;Claus Lamm","doi":"10.1016/j.ynstr.2024.100653","DOIUrl":"10.1016/j.ynstr.2024.100653","url":null,"abstract":"<div><p>Many everyday decisions, including those concerning our health, finances and the environment, involve choosing between a smaller but imminent reward (e.g., €20 now) and a later but larger reward (e.g., €40 in a month). The extent to which an individual prefers smaller imminent rewards over larger delayed rewards can be measured using delay discounting tasks. Acute stress induces a cascade of biological and psychological responses with potential consequences for how individuals think about the future, process rewards, and make decisions, all of which can impact delay discounting. Several studies have shown that individuals focus more on imminent rewards under stress. These findings have been used to explain why individuals make detrimental choices under acute stress. Yet, the evidence linking acute stress to delay discounting is equivocal. To address this uncertainty, we conducted a meta-analysis of 11 studies (14 effects) to systematically quantify the effects of acute stress on monetary delay discounting. Overall, we find no effect of acute stress on delay discounting, compared to control conditions (SMD = −0.18, 95% CI [-0.57, 0.20], p = 0.32). We also find that neither the gender/sex of the participants, the type of stressor (e.g., physical vs. psychosocial) nor whether monetary decisions were hypothetical or incentivized (i.e. monetary decisions were actually paid out) moderated the impact of acute stress on monetary delay discounting. We argue that establishing the effects of acute stress on the separate processes involved in delay discounting, such as reward valuation and prospection, will help to resolve the inconsistencies in the field.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100653"},"PeriodicalIF":5.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000493/pdfft?md5=a2df63aab46e309e647c3480e20c9371&pid=1-s2.0-S2352289524000493-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141280737","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}

{"title":"Hyperexcitation of the glutamatergic neurons in lateral hypothalamus induced by chronic pain contributes to depression-like behavior and learning and memory impairment in male mice","authors":"Lianghui Meng ,&nbsp;Xuefeng Zheng ,&nbsp;Keman Xie,&nbsp;Yifei Li,&nbsp;Danlei Liu,&nbsp;Yuanyuan Xu,&nbsp;Jifeng Zhang,&nbsp;Fengming Wu,&nbsp;Guoqing Guo","doi":"10.1016/j.ynstr.2024.100654","DOIUrl":"10.1016/j.ynstr.2024.100654","url":null,"abstract":"<div><p>Chronic pain can induce mood disorders and cognitive dysfunctions, such as anxiety, depression, and learning and memory impairment in humans. However, the specific neural network involved in anxiety- and depression-like behaviors and learning and memory impairment caused by chronic pain remains poorly understood. In this study, behavioral test results showed that chronic pain induced anxiety- and depression-like behaviors, and learning and memory impairment in male mice. c-Fos immunofluorescence and fiber photometry recording showed that glutamatergic neurons in the LH of mice with chronic pain were selectively activated. Next, the glutamatergic neurons of LH in normal mice were activated using optogenetic and chemogenetic methods, which recapitulates some of the depressive-like behaviors, as well as memory impairment, but not anxiety-like behavior. Finally, inhibition of glutamatergic neurons in the LH of mice with chronic pain, effectively relieved anxiety- and depression-like behaviors and learning and memory impairment. Taken together, our findings suggest that hyperexcitation of glutamatergic neurons in the LH is involved in depression-like behavior and learning and memory impairment induced by chronic pain.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100654"},"PeriodicalIF":5.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S235228952400050X/pdfft?md5=6b0622f56c031da0a2696b424f60f254&pid=1-s2.0-S235228952400050X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141233507","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}

{"title":"Individual longitudinal changes in DNA-methylome identify signatures of early-life adversity and correlate with later outcome","authors":"Annabel K. Short ,&nbsp;Ryan Weber ,&nbsp;Noriko Kamei ,&nbsp;Christina Wilcox Thai ,&nbsp;Hina Arora ,&nbsp;Ali Mortazavi ,&nbsp;Hal S. Stern ,&nbsp;Laura Glynn ,&nbsp;Tallie Z. Baram","doi":"10.1016/j.ynstr.2024.100652","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100652","url":null,"abstract":"<div><p>Adverse early-life experiences (ELA) affect a majority of the world's children. Whereas the enduring impact of ELA on cognitive and emotional health is established, there are no tools to predict vulnerability to ELA consequences in an individual child. Epigenetic markers including peripheral-cell DNA-methylation profiles may encode ELA and provide predictive outcome markers, yet the interindividual variance of the human genome and rapid changes in DNA methylation in childhood pose significant challenges. Hoping to mitigate these challenges we examined the relation of several ELA dimensions to DNA methylation changes and outcome using a within-subject longitudinal design and a high methylation-change threshold.</p><p>DNA methylation was analyzed in buccal swab/saliva samples collected twice (neonatally and at 12 months) in 110 infants. We identified CpGs differentially methylated across time for each child and determined whether they associated with ELA indicators and executive function at age 5. We assessed sex differences and derived a sex-dependent ‘impact score’ based on sites that most contributed to methylation changes.</p><p>Changes in methylation between two samples of an individual child reflected age-related trends and correlated with executive function years later. Among tested ELA dimensions and life factors including income to needs ratios, maternal sensitivity, body mass index and infant sex, unpredictability of parental and household signals was the strongest predictor of executive function. In girls, high early-life unpredictability interacted with methylation changes to presage executive function. Thus, longitudinal, within-subject changes in methylation profiles may provide a signature of ELA and a potential predictive marker of individual outcome.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100652"},"PeriodicalIF":5.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000481/pdfft?md5=0cf553b631bada52c8cfef4dd0c2e6a7&pid=1-s2.0-S2352289524000481-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141292366","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}

{"title":"Adolescent environmental enrichment induces social resilience and alters neural gene expression in a selectively bred rodent model with anxious phenotype","authors":"Angela May O'Connor ,&nbsp;Megan Hastings Hagenauer,&nbsp;Liam Cannon Thew Forrester,&nbsp;Pamela M. Maras,&nbsp;Keiko Arakawa,&nbsp;Elaine K. Hebda-Bauer,&nbsp;Huzefa Khalil,&nbsp;Evelyn R. Richardson,&nbsp;Farizah I. Rob,&nbsp;Yusra Sannah,&nbsp;Stanley J. Watson Jr.,&nbsp;Huda Akil","doi":"10.1016/j.ynstr.2024.100651","DOIUrl":"https://doi.org/10.1016/j.ynstr.2024.100651","url":null,"abstract":"<div><p>Stress is a major influence on mental health status; the ways that individuals respond to or copes with stressors determine whether they are negatively affected in the future. Stress responses are established by an interplay between genetics, environment, and life experiences. Psychosocial stress is particularly impactful during adolescence, a critical period for the development of mood disorders. In this study we compared two established, selectively-bred Sprague Dawley rat lines, the “internalizing” bred Low Responder (bLR) line versus the “externalizing” bred High Responder (bHR) line, to investigate how genetic temperament and adolescent environment impact future responses to social interactions and psychosocial stress, and how these determinants of stress response interact. Male bLR and bHR rats were exposed to social and environmental enrichment in adolescence prior to experiencing social defeat and were then assessed for social interaction and anxiety-like behavior. Adolescent enrichment caused rats to display more social interaction, as well as nominally less social avoidance, less submission during defeat, and resilience to the effects of social stress on corticosterone, in a manner that seemed more notable in bLRs. For bHRs, enrichment also caused greater aggression during a neutral social encounter and nominally during defeat, and decreased anxiety-like behavior. To explore the neurobiology underlying the development of social resilience in the anxious phenotype bLRs, RNA-seq was conducted on the hippocampus and nucleus accumbens, two brain regions that mediate stress regulation and social behavior. Gene sets previously associated with stress, social behavior, aggression and exploratory activity were enriched with differential expression in both regions, with a particularly large effect on gene sets that regulate social behaviors. Our findings provide further evidence that adolescent enrichment can serve as an inoculating experience against future stressors. The ability to induce social resilience in a usually anxious line of animals by manipulating their environment has translational implications, as it underscores the feasibility of intervention strategies targeted at genetically vulnerable adolescent populations.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100651"},"PeriodicalIF":5.0,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S235228952400047X/pdfft?md5=4f4599f39a78873b53a1c34653e282a6&pid=1-s2.0-S235228952400047X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141286296","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}

{"title":"Effects of acute stress on reward processing: A comprehensive meta-analysis of rodent and human studies","authors":"Martino Schettino ,&nbsp;Valeria Tarmati ,&nbsp;Paola Castellano ,&nbsp;Valeria Gigli ,&nbsp;Luca Carnevali ,&nbsp;Simona Cabib ,&nbsp;Cristina Ottaviani ,&nbsp;Cristina Orsini","doi":"10.1016/j.ynstr.2024.100647","DOIUrl":"10.1016/j.ynstr.2024.100647","url":null,"abstract":"<div><p>Stressors can initiate a cascade of central and peripheral changes that modulate mesocorticolimbic dopaminergic circuits and, ultimately, behavioral response to rewards. Driven by the absence of conclusive evidence on this topic and the Research Domain Criteria framework, random-effects meta-analyses were adopted to quantify the effects of acute stressors on reward responsiveness, valuation, and learning in rodent and human subjects.</p><p>In rodents, acute stress reduced reward responsiveness (<em>g</em> = −1.43) and valuation (<em>g</em> = −0.32), while amplifying reward learning (<em>g</em> = 1.17). In humans, acute stress had marginal effects on valuation (<em>g</em> = 0.25), without affecting responsiveness and learning. Moderation analyses suggest that acute stress neither has unitary effects on reward processing in rodents nor in humans and that the duration of the stressor and specificity of reward experience (i.e., food vs drugs) may produce qualitatively and quantitatively different behavioral endpoints.</p><p>Subgroup analyses failed to reduce heterogeneity, which, together with the presence of publication bias, pose caution on the conclusions that can be drawn and point to the need of guidelines for the conduction of future studies in the field.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100647"},"PeriodicalIF":5.0,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000432/pdfft?md5=99670d9ad52837144ea285d4c1bf4f65&pid=1-s2.0-S2352289524000432-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141139398","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}

{"title":"Brain correlates and functional connectivity linking stress, autonomic dysregulation, and alcohol motivation","authors":"Dongju Seo ,&nbsp;Jorge S. Martins ,&nbsp;Rajita Sinha","doi":"10.1016/j.ynstr.2024.100645","DOIUrl":"10.1016/j.ynstr.2024.100645","url":null,"abstract":"<div><p>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 &lt; 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 &lt; 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.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100645"},"PeriodicalIF":5.0,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000419/pdfft?md5=3a245b2128a6213077f2e1182d6f1cbb&pid=1-s2.0-S2352289524000419-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141136597","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}

{"title":"Omega-3 alleviates behavioral and molecular changes in a mouse model of stress-induced juvenile depression","authors":"Tatyana Strekalova ,&nbsp;Daniel Radford-Smith ,&nbsp;Isobel K. Dunstan ,&nbsp;Anna Gorlova ,&nbsp;Evgeniy Svirin ,&nbsp;Elisaveta Sheveleva ,&nbsp;Alisa Burova ,&nbsp;Sergey Morozov ,&nbsp;Aleksey Lyundup ,&nbsp;Gregor Berger ,&nbsp;Daniel C. Anthony ,&nbsp;Susanne Walitza","doi":"10.1016/j.ynstr.2024.100646","DOIUrl":"10.1016/j.ynstr.2024.100646","url":null,"abstract":"<div><h3>Introduction</h3><p>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.</p></div><div><h3>Methods</h3><p>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.</p></div><div><h3>Results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100646"},"PeriodicalIF":5.0,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000420/pdfft?md5=ae79e6addcc1c3641fd5e4579f15a922&pid=1-s2.0-S2352289524000420-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141144721","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}

{"title":"The role of resilience in the relationship between stress and alcohol","authors":"Melanie L. Schwandt ,&nbsp;Eva Cullins ,&nbsp;Vijay A. Ramchandani","doi":"10.1016/j.ynstr.2024.100644","DOIUrl":"10.1016/j.ynstr.2024.100644","url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100644"},"PeriodicalIF":5.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000407/pdfft?md5=8641d237fceab69ab6cc4d3b927d56c3&pid=1-s2.0-S2352289524000407-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141023230","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}

{"title":"Coffee polyphenols ameliorate early-life stress-induced cognitive deficits in male mice","authors":"J. Geertsema ,&nbsp;M. Kratochvil ,&nbsp;R. González-Domínguez ,&nbsp;S. Lefèvre-Arbogast ,&nbsp;D.Y. Low ,&nbsp;A. Du Preez ,&nbsp;H. Lee ,&nbsp;M. Urpi-Sarda ,&nbsp;A. Sánchez-Pla ,&nbsp;L. Aigner ,&nbsp;C. Samieri ,&nbsp;C. Andres-Lacueva ,&nbsp;C. Manach ,&nbsp;S. Thuret ,&nbsp;P.J. Lucassen ,&nbsp;A. Korosi","doi":"10.1016/j.ynstr.2024.100641","DOIUrl":"10.1016/j.ynstr.2024.100641","url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"31 ","pages":"Article 100641"},"PeriodicalIF":5.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000377/pdfft?md5=40d2abee4459a0f3845da654a524f7d4&pid=1-s2.0-S2352289524000377-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141051629","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}