Neurobiology of Stress最新文献

{"title":"Resilience in motion: emerging perspectives on stress, substance use and youth","authors":"P. Sampedro-Piquero","doi":"10.1016/j.ynstr.2026.100783","DOIUrl":"10.1016/j.ynstr.2026.100783","url":null,"abstract":"<div><div>Adolescence and young adulthood are developmental stages characterized by heightened stress sensitivity and limited cognitive control. The identification of the risk factors of alcohol consumption in these stages is crucial for early interventions focused on reducing harmful alcohol use. This review examines how exercise can modulate stress responses, reduce cravings, and preserve cognitive and emotional functioning. In animal models, it has been well described that exercise is able to reduce craving and protect cognitive and affective domains. Translational studies in young people with risky alcohol use (RAU) revealed comparable benefits. Acute aerobic exercise improved executive functions, such as verbal fluency, whereas stretching induced distinct neural oscillatory changes related to emotion regulation. These findings underscore the heterogeneous yet complementary effects of different exercise modalities, suggesting that tailored interventions may optimize outcomes. Future work will incorporate interoceptive measures to clarify the mechanisms linking stress dysregulation and RAU vulnerability, with particular attention to gender-related differences. Collectively, the evidence suggests that aerobic exercise may constitute a promising, feasible, and transdiagnostic intervention that strengthens stress-response systems, reduces craving, and fosters resilience in young people at risk of alcohol misuse, with women showing interoceptive deficits emerging as a particularly vulnerable subgroup.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"41 ","pages":"Article 100783"},"PeriodicalIF":3.6,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146081238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the cellular landscape of biological stress in the human brain","authors":"Natalie Matosin","doi":"10.1016/j.ynstr.2026.100782","DOIUrl":"10.1016/j.ynstr.2026.100782","url":null,"abstract":"<div><div>Adversity exposure leading to a dysfunctional biological stress response represents a significant risk factor underlying psychiatric disorder aetiology for many individuals. Yet our understanding of how different cell types within stress-responsive brain circuits differentially contribute to psychiatric risk remains limited, particularly in the human brain. Our lab, the Mental Illness, Neurobiology and Disorders of Stress (MINDS) Laboratory, has been addressing this knowledge gap through large-scale analyses of postmortem human brain specimens from individuals with major psychiatric disorders who experienced high levels of adversity in their lives. We have a focus on examining targets and pathways involved in HPA axis and glucocorticoid-mediated signalling in the human brain at single-cell resolution. Through integration of single-cell and spatial molecular data with advanced histological approaches to evaluate cellular morphology, we have identified cell-type-specific vulnerability patterns to the biological consequences of adversity exposure. Our findings demonstrate how different populations respond to adversity through coordinated molecular and morphological changes that affect synaptic function and stability. This approach exemplifies the potential for combining new spatial omics and traditional histological approaches to achieve precision medicine in psychiatry, by revealing specific cellular targets for therapeutic intervention. Our work facilitates a shift from broad neurotransmitter-based interventions towards targeted therapeutic strategies for stress-related psychiatric disorders. These advances provide a foundation for developing more effective treatments tailored to the underlying cellular pathology in individual patients with stress-related mental illness.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"41 ","pages":"Article 100782"},"PeriodicalIF":3.6,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroplacentology of stress: Novel frontiers linking maternal mental health to offspring neurodevelopment","authors":"Cristiana Cruceanu","doi":"10.1016/j.ynstr.2025.100778","DOIUrl":"10.1016/j.ynstr.2025.100778","url":null,"abstract":"<div><div>Neuroplacentology is an emerging interdisciplinary field integrating molecular neuroscience, placental biology, environmental modeling, and single-cell techniques to study stress-related neurodevelopmental programming. The placenta, once considered merely a conduit between mother and fetus, is now recognized as an important regulator of fetal brain development and a mediator of prenatal maternal stress and other exposures. To highlight this important aspect of the neurobiology of stress, this review outlines how maternal stress, genetic susceptibility, and environmental exposures converge at the placenta-brain axis to influence offspring psychiatric vulnerability.</div><div>Risk and resilience for psychiatric conditions are shaped by interactions between genetic predisposition and environmental exposures, including during the highly plastic prenatal period. Prenatal stress exposure can alter neuronal differentiation, transcription factor gene-regulatory networks, and excitation/inhibition neuronal balance. In parallel, maternal metabolic disorders, placental endocrine dysregulation, and psychotropic medication exposure modulate neuroactive pathways critical to brain development. The placenta responds to these exposures and synthesizes key stress molecules such as corticotropin-releasing hormone, serotonin and other neuromodulators, highlighting its neuroregulatory role.</div><div>To exemplify the promising future of neuroplacentology for our understanding of perinatal health and stress research, this review highlights innovative methodological approaches such as human-specific placental organoid systems and single-cell multi-omics. I propose that future research should focus on identifying placental biomarkers predictive of neurodevelopmental outcomes and refining <em>in-vitro</em> models for testing pharmacological interventions in a non-invasive manner. Elucidating the mechanisms at the placenta-brain interface, could lead to a better understanding of the developmental origins of mental illness and inform early intervention strategies.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100778"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ventral pallidum GABA neuron inhibition augments context-appropriate defensive responses to learned threat cues","authors":"Erica M. Ramirez ,&nbsp;Maricela X. Martinez ,&nbsp;Ryan K. Rokerya ,&nbsp;Vanessa Alizo Vera ,&nbsp;Christina M. Ruiz ,&nbsp;Mitchell R. Farrell ,&nbsp;Shreeya A. Walawalkar ,&nbsp;Hazael Ramirez-Ramirez ,&nbsp;Grace J. Kollman ,&nbsp;Stephen V. Mahler","doi":"10.1016/j.ynstr.2026.100781","DOIUrl":"10.1016/j.ynstr.2026.100781","url":null,"abstract":"<div><div>The ventral pallidum (VP) is embedded within the brain circuits controlling motivated behavior, which are heavily implicated in addiction and other psychiatric disorders. Prior work showed that VP GABAergic neurons (VP^GABA) promote reward approach and seeking, while the intermixed population of VP glutamate neurons instead promote avoidance and aversion. Some have thus suggested a functional dichotomy between these VP subpopulations in reward versus threat. We test this hypothesis by asking how inhibiting VP^GABA impacts active and passive defensive responses to learned threat cues in the absence of rewards. We taught GAD1:Cre rats with inhibitory VP^GABA DREADDs (or control rats) that a metal probe delivers shock, or that a 20sec auditory cue precedes footshocks. These stimuli thereafter elicit active defensive burying, or passive freezing responses, respectively. We found that VP^GABA inhibition with CNO markedly increased stimulus-appropriate defensive responses to both types of learned threats, but failed to consistently alter new learning about them—suggesting VP^GABA mediates aversive motivation but not memory formation. VP^GABA inhibition also altered threat-related c-Fos expression within VP cell populations, and in their efferent target lateral habenula, but not mediodorsal thalamus—pointing to potential underlying circuit mechanisms of defensive responses. Results indicate that VP^GABA neurons not only promote reward seeking as previously reported, but that they may also actively inhibit defensive responses to threats that might otherwise compete with reward seeking. This refines our understanding of subcortical valanced motivation circuits, and may suggest new targets for intervening in disorders like addiction and depression.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100781"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adolescent adversity persistently induces proinflammatory HMGB1 signaling and disrupts the basal forebrain cholinergic system in female rats","authors":"Hayley Ross ,&nbsp;Makayla Adelman ,&nbsp;Juan E. Castillo ,&nbsp;Ann Walker ,&nbsp;Joseph Latham ,&nbsp;Liya Qin ,&nbsp;Victoria Macht ,&nbsp;Fulton T. Crews ,&nbsp;Ryan P. Vetreno","doi":"10.1016/j.ynstr.2025.100779","DOIUrl":"10.1016/j.ynstr.2025.100779","url":null,"abstract":"<div><div>Adolescence is a critical period of neurodevelopment characterized by heightened neuroplasticity and refinement of executive functioning and cognition. Basal forebrain cholinergic neurons mature during this period, coinciding with development of adult cognitive function. Exposure to adolescent adversity has been linked to long-lasting neurobiological and cognitive consequences, yet the mechanisms underlying these outcomes remain poorly understood. Using a preclinical model of adolescent intermittent restraint stress (AIRS), we tested the hypothesis that adolescent adversity induces lasting proinflammatory innate immune signaling, loss of basal forebrain cholinergic neurons, and cognitive deficits in adult female rats. We report that AIRS elevated plasma levels of corticosterone and proinflammatory high mobility group box 1 (HMGB1), consistent with HPA axis activation and systemic inflammation. In the late adolescent (P55) basal forebrain, AIRS caused an increase of the proinflammatory signaling molecule HMGB1, the HMGB1 receptors TLR4 and RAGE, the downstream proinflammatory transcription activation marker pNF-κB p65, and proinflammatory cytokines that persisted into adulthood (P95). This was accompanied by persistent adult increases of microglial activation markers, Iba-1 and CD11b. Importantly, AIRS caused a reduction of ChAT+ and TrkA + basal forebrain cholinergic neurons that persisted into adulthood, paralleling significant impairments in recognition memory on the novel object recognition memory test. Together, these findings suggest that adolescent adversity induces persistent proinflammatory HMGB1-TLR4/RAGE-pNF-κB signaling, microglial priming, and reductions of basal forebrain cholinergic neurons as well as enduring cognitive impairment. The HMGB1 proinflammatory pathway may represent a promising therapeutic target for mitigating the long-term neurobiological and behavioral consequences of adolescent adversity.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100779"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Central amygdala Fkbp5 expression correlates with faster submission and ethanol self-administration reacquisition: Benztropine reduces ethanol relapse-like reacquisition in stressed rats","authors":"Luisa B. Bertotto ,&nbsp;Eleanna M. Sakoulas ,&nbsp;Marian L. Logrip ,&nbsp;Katrina Lin ,&nbsp;Anastasia E. Pimentel ,&nbsp;Lenwood Thompson ,&nbsp;Bryan Cruz ,&nbsp;Valentina Vozella ,&nbsp;Cristiane A. Favoretto ,&nbsp;Marisa Roberto ,&nbsp;Eric P. Zorrilla","doi":"10.1016/j.ynstr.2025.100770","DOIUrl":"10.1016/j.ynstr.2025.100770","url":null,"abstract":"<div><div>Stress-related emotional disorders, such as post-traumatic stress disorder (PTSD) and major depression, increase alcohol relapse risk. PTSD, depression, and alcohol use phenotypes associate with gene variants of FKBP prolyl isomerase 5 (<em>FKBP5</em>), a chaperone modulator of glucocorticoid receptors (GR). FKBP51 inhibitors can decrease ethanol intake, but FKBP51's role in recurrence of post-stress ethanol drinking is unknown. We tested the hypotheses that expression of <em>Fkbp5</em> and immediate early genes (IEGs) in the central nucleus of the amygdala (CeA) is increased in rats with a history of defeat or foot-shock stress and associates with faster submission and increased reacquisition of ethanol self-administration. We tested if benztropine mesylate, an FDA-approved drug that inhibits FKBP51-GR binding, reduces reacquisition of ethanol self-administration in rats with a history of foot-shock stress. Wistar rats were studied after resident-intruder social defeat (<em>n</em> = 32) or in an ethanol self-administration reacquisition model, with or without repeated foot-shock history (<em>n</em> = 62). Acute social defeat stress increased CeA IEG expression within 1 h <em>Fkbp5</em> expression by 6 h. CeA IEG activation correlated with <em>Fkbp5</em> expression, and both correlated with faster submission to defeat. CeA <em>Fkbp5</em> expression also associated with greater ethanol intake and blood ethanol concentration during reacquisition of ethanol self-administration. Benztropine (i.p., 5, 10 mg/kg) dose-dependently reduced relapse-like ethanol reacquisition, and sex-specific analyses suggest a more robust effect in males than females. The results warrant the study of CeA FKBP51 in passive stress coping and of drug-like selective FKBP51 inhibitors to reduce ethanol relapse after histories of repeated stress.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100770"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental and early-life stress-induced effects on 5-HT3R-expressing interneurons within auditory cortex","authors":"James T. Moore ,&nbsp;Matthew J. Sunthimer ,&nbsp;Ethan White ,&nbsp;Jeffrey G. Mellott ,&nbsp;Merri J. Rosen","doi":"10.1016/j.ynstr.2026.100780","DOIUrl":"10.1016/j.ynstr.2026.100780","url":null,"abstract":"<div><div>Early life stress (ELS) is a well-known predictor of neuropsychiatric disease and contributes to the development of sensory processing deficits that persist throughout life. Organisms are particularly susceptible to the deleterious effects of stress during critical periods, when neuroplasticity is heightened, and initial representations of the sensory environment are mapped to cortex. When ELS is induced during the auditory cortical (ACx) critical period, it impairs both neural and behavioral responses to a variety of auditory stimuli that rely on temporal processing. Mechanisms by which ELS may alter critical period plasticity are of particular interest in understanding ELS-related pathology, including the 5-HT3R interneuron system, which has been implicated in regulating neural activity during critical periods. Here we examined two principal subpopulations of interneurons in primary ACx: VIP and NDNF cells, which account for a majority of cortical neurons expressing 5-HT3R. The expression of the Htr3a gene during normal development and under ELS conditions was quantified using multiplex fluorescent <em>in situ</em> hybridization. We show that densities of cells expressing NDNF and VIP decrease following ear opening and across the ACx critical period, and that ELS results in the maintenance of elevated cell densities compared to age-matched controls. Further, Htr3a in VIP neurons is developmentally upregulated, and its expression is further increased by ELS beyond normal physiologic levels. Stress-induced shifts in these serotonergic interneurons may contribute to deficits that arise in auditory cortical and perceptual responses via effects on local cortical circuitry.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100780"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics reveals associations between the microbiota-gut-brain axis and antidepressant effects of vagus nerve stimulation","authors":"Dan Pan ,&nbsp;Mingchen Jiang ,&nbsp;Ying Wang ,&nbsp;Junyuan He ,&nbsp;Jumei Tang ,&nbsp;Siyu Liu ,&nbsp;Mingxia Li ,&nbsp;Xing Jiang ,&nbsp;Qiuyue Xu","doi":"10.1016/j.ynstr.2025.100777","DOIUrl":"10.1016/j.ynstr.2025.100777","url":null,"abstract":"<div><h3>Background</h3><div>Major depressive disorder is a severe mental health condition characterized by persistent depressed mood and loss of interest. Current first-line pharmacotherapies often exhibit limited therapeutic performance and adverse side effects. Transcutaneous auricular vagus nerve stimulation (taVNS) is a promising, safe, and noninvasive alternative intervention with demonstrated neuromodulatory efficacy. Nevertheless, its mechanisms remain unclear. This study investigated whether the antidepressant properties of taVNS are associated with the microbiota-gut-brain axis, focusing on the potential crosstalk between differentially expressed hippocampal proteins and the gut microbiota.</div></div><div><h3>Methods</h3><div>A chronic unpredictable mild stress (CUMS) rat model of depression was established, and taVNS was administered for 14 days. Hippocampal proteomic profiling was performed using data-independent acquisition. Fecal metagenomic sequencing was conducted to characterize alterations in gut microbial communities. Key signaling pathways were validated using Western blot, qRT-PCR, HE staining, and transmission electron microscopy, all of which were employed to systematically assess behavioral, proteomic, microbial, and molecular changes.</div></div><div><h3>Results</h3><div>Proteomics and molecular analyses revealed that taVNS upregulated hippocampal expression of glutamate ionotropic receptor N-methyl-D-aspartate type subunit 1 (GluN1) and brain-derived neurotrophic factor (BDNF), while simultaneously restoring mitogen-activated protein kinase (MAPK) signaling activity. Metagenomic profiling demonstrated that taVNS increased the abundance of <em>Akkermansia muciniphila</em> and reduced <em>Ligilactobacillus reuteri</em>. Ligilactobacillus levels were positively correlated with synaptogyrin-1 (Syngr1), indicating their potential association in enhancing the antidepressant effects mediated by the GluN1/MAPK/BDNF signaling cascade.</div></div><div><h3>Conclusion</h3><div>TaVNS significantly alleviated depression-like behaviors in CUMS-exposed rats. The underlying mechanism may involve the restoration of synaptic function of glutamatergic neurons by regulating the GluN1/MAPK/BDNF signaling pathway. In addition, taVNS reshaped the gut microbiota, markedly increasing the abundance of <em>Akkermansia muciniphila</em> and <em>Ligilactobacillus murinus</em> while reducing <em>Limosilactobacillus reuteri</em> and <em>Lactobacillus johnsonii</em>. The positive correlation between Syngr1 protein level and Ligilactobacillus abundance in the hippocampus suggests that the microbiota-gut-brain axis may play a key role in the antidepressant effects of taVNS.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100777"},"PeriodicalIF":3.6,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145734391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hair stress hormones in individuals with a recent suicide attempt experiencing a depressive episode","authors":"Lejla Colic ,&nbsp;Anna Karoline Seiffert ,&nbsp;Lydia Bahlmann ,&nbsp;Ani Zerekidze ,&nbsp;Johanna Walther ,&nbsp;Larissa McClain ,&nbsp;Bianca Besteher ,&nbsp;Fabricio Pereira ,&nbsp;Mocrane Abbar ,&nbsp;Martin Walter ,&nbsp;Fabrice Jollant ,&nbsp;Gerd Wagner","doi":"10.1016/j.ynstr.2025.100776","DOIUrl":"10.1016/j.ynstr.2025.100776","url":null,"abstract":"<div><h3>Background</h3><div>Stressful events and dysregulation of the hypothalamic-pituitary-adrenal (HPA)- axis contribute to the risk of suicide attempt (SA) in persons in depressive episodes. Hair cortisol, cortisone and dehydroepiandrosterone (DHEA) concentrations may serve as reliable indicators of HPA axis dysregulation prior to SA.</div></div><div><h3>Methods</h3><div>Participants (n = 75; mean age [standard deviation] = 30.0 [10.2] years; n = 49 [65 %] women; Jena site) comprised three groups: individuals with a history of SA approximately one month (SA; n = 22); individuals with a current depressive episode without SA history (CC; n = 31) and healthy individuals (HC; n = 22). SA was defined as self-initiated, potentially injurious behavior accompanied by some intent to die. Stress hormones were measured using LC-MS/MS protocol (days from sampling to analysis = 342 [171]) and logarithmic transformed. Group differences in hair stress hormones with hair segments representing time were tested using linear mixed models on a p &lt; .05 threshold. Exploratory models further examined the effects of childhood abuse, frequency of SAs, suicide intent level and impulsiveness of the last SA of mean hormone levels, on a corrected p_corr&lt; .012 threshold.</div></div><div><h3>Results</h3><div>There was a main effect of group for the DHEA-log (p = .02) and post-hoc tests indicated that SA group had higher DHEA compared to CC (p_corr = .01) and HC (p_corr = .08) in the peri-suicidal period. There were no significant (p &lt; .05) interaction or group effects on cortisol-log and cortisone-log. Preliminary exploratory analyses showed that SA with multiple attempts had higher mean DHEA-log compared to SA with a single suicide attempt (p_uncorr = .05). Furthermore, there were positive associations between level of suicide intent and both mean cortisol-log (p_uncorr = .02) and mean cortisone-log (p_uncorr = .02). Childhood abuse and impulsiveness of the last SA were not related to hair stress hormones.</div></div><div><h3>Conclusions</h3><div>Individuals with a recent history of SA showed alterations in the DHEA hair levels. These results partially support dysregulation of the HPA axis as a biopsychosocial feature of SA. Future longitudinal and experimental studies should investigate whether hair HPA axis hormones can serve as markers of suicidal crisis and vulnerability.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100776"},"PeriodicalIF":3.6,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-dependent effects of chronic traumatic and social isolation stress on mice social behavior","authors":"Moonseok Choi ,&nbsp;Jisu Jeong ,&nbsp;Dongsoo Kim ,&nbsp;Hong Seok Choi ,&nbsp;Junghwa Ryu ,&nbsp;Hye Jin Choi ,&nbsp;Mookyung Cheon ,&nbsp;Yun Ha Jeong","doi":"10.1016/j.ynstr.2025.100773","DOIUrl":"10.1016/j.ynstr.2025.100773","url":null,"abstract":"<div><div>Modern people are exposed to various stressful situations. Stress is a significant factor in emotional changes and social behavior and is associated with imbalances in physiological and psychological homeostasis, including brain function and structure. Stress has multiple causes, each of which has different impacts on social behavior throughout life. However, little is known about how stress influences social behavior across the life cycle. To understand this further, this study exposed mice to chronic stress at three different ages: adolescence, early adulthood, and adulthood. Chronic stresses were induced by combining chronic traumatic and isolation stress. Chronic stress has been shown to enhance social dominance behavior, especially in adolescence, and changes in the expression of genes and proteins, including Fabp7 and Cxcl12, were observed to change in the opposite direction compared to adulthood, confirming that it is related to changes in social dominance behavior. This study may provide important insights into factors related to adolescence social behavior abnormalities.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"40 ","pages":"Article 100773"},"PeriodicalIF":3.6,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}