Neurobiology of Stress最新文献

{"title":"Imaging a putative marker of brain cortisol regulation in alcohol use disorder","authors":"Terril L. Verplaetse ,&nbsp;Ansel T. Hillmer ,&nbsp;Shivani Bhatt ,&nbsp;Aleksandra Rusowicz ,&nbsp;Songye Li ,&nbsp;Nabeel Nabulsi ,&nbsp;David Matuskey ,&nbsp;Yiyun Huang ,&nbsp;Sherry A. McKee ,&nbsp;Kelly P. Cosgrove","doi":"10.1016/j.ynstr.2024.100609","DOIUrl":"10.1016/j.ynstr.2024.100609","url":null,"abstract":"<div><h3>Background</h3><p>Stress is a potent activator of the hypothalamic-pituitary-adrenal (HPA) axis, initiating the release of glucocorticoid hormones, such as cortisol. Alcohol consumption can lead to HPA axis dysfunction, including altered cortisol levels. Until recently, research has only been able to examine peripheral cortisol associated with alcohol use disorder (AUD) in humans. We used positron emission tomography (PET) brain imaging with the radiotracer [¹⁸F]AS2471907 to measure 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), a cortisol-regenerating enzyme, in people with AUD compared to healthy controls.</p></div><div><h3>Methods</h3><p>We imaged 9 individuals with moderate to severe AUD (5 men, 4 women; mean age = 38 years) and 12 healthy controls (8 men, 4 women; mean age = 29 years). Participants received 93.5 ± 15.6 MBq of the 11β-HSD1 inhibitor radiotracer [¹⁸F]AS2471907 as a bolus injection and were imaged for 150–180 min on the High-Resolution Research Tomograph. 11β-HSD1 availability was quantified by [¹⁸F]AS2471907 volume of distribution (<em>V</em>_T; mL/cm³). <em>A priori</em> regions of interest included amygdala, anterior cingulate cortex (ACC), hippocampus, ventromedial PFC (vmPFC) and caudate.</p></div><div><h3>Results</h3><p>Individuals with AUD consumed 52.4 drinks/week with 5.8 drinking days/week. Healthy controls consumed 2.8 drinks/week with 1.3 drinking days/week. Preliminary findings suggest that [¹⁸F]AS2471907 <em>V</em>_T was higher in amygdala, ACC, hippocampus, vmPFC, and caudate of those with AUD compared to healthy controls (<em>p</em> &lt; 0.05). In AUD, vmPFC [¹⁸F]AS2471907 <em>V</em>_T was associated with drinks per week (r = 0.81, <em>p</em> = 0.01) and quantity per drinking episode (r = 0.75, <em>p</em> = 0.02).</p></div><div><h3>Conclusions</h3><p>This is the first <em>in vivo</em> examination of 11β-HSD1 availability in individuals with AUD. Our data suggest higher brain availability of the cortisol-regenerating enzyme 11β-HSD1 in people with AUD (vs. controls), and that higher vmPFC 11β-HSD1 availability is related to greater alcohol consumption. Thus, in addition to the literature suggesting that people with AUD have elevated peripheral cortisol, our findings suggest there may also be heightened central HPA activity. These findings set the foundation for future hypotheses on mechanisms related to HPA axis function in this population.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100609"},"PeriodicalIF":5.0,"publicationDate":"2024-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000055/pdfft?md5=2ad0ca0c2b05a36a7d0a86365f2daa6f&pid=1-s2.0-S2352289524000055-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139539676","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":"Early resource scarcity causes cortical astrocyte enlargement and sex-specific changes in the orbitofrontal cortex transcriptome in adult rats","authors":"Claire Deckers ,&nbsp;Reza Karbalaei ,&nbsp;Nylah A. Miles ,&nbsp;Eden V. Harder ,&nbsp;Emily Witt ,&nbsp;Erin P. Harris ,&nbsp;Kathryn Reissner ,&nbsp;Mathieu E. Wimmer ,&nbsp;Debra A. Bangasser","doi":"10.1016/j.ynstr.2024.100607","DOIUrl":"10.1016/j.ynstr.2024.100607","url":null,"abstract":"<div><p>Astrocyte morphology affects function, including the regulation of glutamatergic signaling. This morphology changes dynamically in response to the environment. However, how early life manipulations alter adult cortical astrocyte morphology is underexplored. Our lab uses brief postnatal resource scarcity, the limited bedding and nesting (LBN) manipulation, in rats. We previously found that LBN augments maternal behaviors and promotes later resilience to adult addiction-related behaviors, reducing impulsivity, risky decision-making, and morphine self-administration. These behaviors rely on glutamatergic transmission in the medial orbitofrontal (mOFC) and medial prefrontal (mPFC) cortex. Here we tested whether LBN changed astrocyte morphology in the mOFC and mPFC of adult rats using a novel viral approach that, unlike traditional markers, fully labels astrocytes. Prior exposure to LBN causes an increase in the surface area and volume of astrocytes in the mOFC and mPFC of adult males and females relative to control-raised rats. We next used bulk RNA sequencing of OFC tissue to assess transcriptional changes that could increase astrocyte size in LBN rats. LBN caused mainly sex-specific changes in differentially expressed genes. Pathway analysis revealed that OFC glutamatergic signaling is altered by LBN in males and females, but the gene changes in that pathway differed across sex. This may represent a convergent sex difference where glutamatergic signaling, which affects astrocyte morphology, is altered by LBN via sex-specific mechanisms. Collectively, these studies highlight that astrocytes may be an important cell type that mediates the effect of early resource scarcity on adult brain function.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100607"},"PeriodicalIF":5.0,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000031/pdfft?md5=e66276def98c8a6053aa3e3c05353b8f&pid=1-s2.0-S2352289524000031-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139469195","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":"Fear conditioning and extinction distinctively alter bidirectional synaptic plasticity within the amygdala of an animal model of post-traumatic stress disorder","authors":"Kwanghoon Park,&nbsp;Hoyong Park,&nbsp;ChiHye Chung","doi":"10.1016/j.ynstr.2024.100606","DOIUrl":"10.1016/j.ynstr.2024.100606","url":null,"abstract":"<div><p>Synaptic plasticity in the amygdala plays an essential role in the formation and inhibition of fear memory; however, this plasticity has mainly been studied in the lateral amygdala, making it largely uninvestigated in other subnuclei. Here, we investigated long-term potentiation (LTP) and long-term depression (LTD) in the basolateral amygdala (BLA) to the medial division of the central amygdala (CEm) synapses of juvenile C57BL/6N (B6) and 129S1/SvImJ (S1) mice. We found that in naïve B6 and S1 mice, LTP was not induced at the BLA to CEm synapses, whereas fear conditioning lowered the threshold for LTP induction in these synapses of both B6 and S1 mice. Interestingly, fear extinction disrupted the induction of LTP at the BLA to CEm synapses of B6 mice, whereas LTP was left intact in S1 mice. Both low-frequency stimulation (LFS) and modest LFS (mLFS) induced LTD in naïve B6 and S1 mice, suggesting that the BLA to CEm synapses express bidirectional plasticity. Fear conditioning disrupted both types of LTD induction selectively in S1 mice and LFS-LTD, presumably NMDAR-dependent LTD was partially recovered by fear extinction. However, mLFS-LTD which has been known to be endocannabinoid receptor 1 (CB1R)-dependent was not induced after fear extinction in both mouse strains. Our observations suggest that fear conditioning enhances LTP while fear extinction diminishes LTP at the BLA to the CEm synapses of B6 mice with successful extinction. Considering that S1 mice showed strong fear conditioning and impaired extinction, strong fear conditioning in the S1 strain may be related to disrupted LTD, and impaired extinction may be due to constant LTP and weak LFS-LTD at the BLA to CEm synapses. Our study contributes to the further understanding of the dynamics of synaptic potentiation and depression between the subnuclei of the amygdala in juvenile mice after fear conditioning and extinction.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100606"},"PeriodicalIF":5.0,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S235228952400002X/pdfft?md5=efc33c66b1b819d4579e8e5cb8495837&pid=1-s2.0-S235228952400002X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139437866","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":"A reverse translational study of PPAR-α agonist efficacy in human and rodent models relevant to alcohol use disorder","authors":"Barbara J. Mason ,&nbsp;David Estey ,&nbsp;Amanda Roberts ,&nbsp;Giordano de Guglielmo ,&nbsp;Olivier George ,&nbsp;John Light ,&nbsp;Mike Stoolmiller ,&nbsp;Susan Quello ,&nbsp;Michael Skinner ,&nbsp;Farhad Shadan ,&nbsp;Adnan Begovic ,&nbsp;Mark C. Kyle ,&nbsp;R. Adron Harris","doi":"10.1016/j.ynstr.2023.100604","DOIUrl":"10.1016/j.ynstr.2023.100604","url":null,"abstract":"<div><p>Alcohol Use Disorder (AUD) is a chronic relapsing disorder affecting an estimated 283 million individuals worldwide, with substantial health and economic consequences. Peroxisome proliferator-activated receptors (PPARs), particularly PPAR-α and PPAR-γ, have shown promise in preclinical studies as potential therapeutic targets for AUD. In this human laboratory study, we aimed to translate preclinical findings on the PPAR-α agonist fenofibrate to a human population with current AUD. We hypothesized that, relative to placebo, fenofibrate at the highest FDA-approved dose of 145 mg/d would attenuate responsiveness to <em>in vivo</em> alcohol cues in the lab and reduce drinking under natural conditions. However, the results did not show significant differences in craving and alcohol consumption between the fenofibrate and placebo groups. Reverse translational studies in rodent models confirmed the lack of fenofibrate effect at human-equivalent doses. These findings suggest that inadequate translation of drug dose from rodents to humans may account for the lack of fenofibrate effects on alcohol craving and consumption in humans with AUD. The results highlight the need for new brain-penetrant PPAR-α agonists to adequately test the therapeutic potential of PPAR-α agonists for AUD, and the importance of reverse translational approaches and selection of human-equivalent doses in drug development.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100604"},"PeriodicalIF":5.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289523000929/pdfft?md5=93cc59a2d8f4ecbc4279f315ca745ee6&pid=1-s2.0-S2352289523000929-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139105554","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":"Alcohol and stress exposure across the lifespan are key risk factors for Alzheimer's Disease and cognitive decline","authors":"Laurel R. Seemiller ,&nbsp;Julio Flores-Cuadra ,&nbsp;Keith R. Griffith ,&nbsp;Grace C. Smith ,&nbsp;Nicole A. Crowley","doi":"10.1016/j.ynstr.2024.100605","DOIUrl":"10.1016/j.ynstr.2024.100605","url":null,"abstract":"<div><p>Alzheimer's Disease and related dementias (ADRD) are an increasing threat to global health initiatives. Efforts to prevent the development of ADRD require understanding behaviors that increase and decrease risk of neurodegeneration and cognitive decline, in addition to uncovering the underlying biological mechanisms behind these effects. Stress exposure and alcohol consumption have both been associated with increased risk for ADRD in human populations. However, our ability to understand causal mechanisms of ADRD requires substantial preclinical research. In this review, we summarize existing human and animal research investigating the connections between lifetime stress and alcohol exposures and ADRD.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100605"},"PeriodicalIF":5.0,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289524000018/pdfft?md5=a935ae5f0ec8338fca1bbbc1541100e7&pid=1-s2.0-S2352289524000018-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139093036","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":"Inter- and transgenerational heritability of preconception chronic stress or alcohol exposure: Translational outcomes in brain and behavior","authors":"Rachel C. Rice ,&nbsp;Daniela V. Gil ,&nbsp;Annalisa M. Baratta ,&nbsp;Remy R. Frawley ,&nbsp;Shirley Y. Hill ,&nbsp;Sean P. Farris ,&nbsp;Gregg E. Homanics","doi":"10.1016/j.ynstr.2023.100603","DOIUrl":"10.1016/j.ynstr.2023.100603","url":null,"abstract":"<div><p>Chronic stress and alcohol (ethanol) use are highly interrelated and can change an individual’s behavior through molecular adaptations that do not change the DNA sequence, but instead change gene expression. A recent wealth of research has found that these nongenomic changes can be transmitted across generations, which could partially account for the “missing heritability” observed in genome-wide association studies of alcohol use disorder and other stress-related neuropsychiatric disorders. In this review, we summarize the molecular and behavioral outcomes of nongenomic inheritance of chronic stress and ethanol exposure and the germline mechanisms that could give rise to this heritability. In doing so, we outline the need for further research to: (1) Investigate individual germline mechanisms of paternal, maternal, and biparental nongenomic chronic stress- and ethanol-related inheritance; (2) Synthesize and dissect cross-generational chronic stress and ethanol exposure; (3) Determine cross-generational molecular outcomes of preconception ethanol exposure that contribute to alcohol-related disease risk, using cancer as an example. A detailed understanding of the cross-generational nongenomic effects of stress and/or ethanol will yield novel insight into the impact of ancestral perturbations on disease risk across generations and uncover actionable targets to improve human health.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100603"},"PeriodicalIF":5.0,"publicationDate":"2023-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289523000917/pdfft?md5=f01b34800cc2eadfd0001cc2e63a9cb4&pid=1-s2.0-S2352289523000917-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139071837","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":"An epigenetic mechanism of social isolation stress in adolescent female mice","authors":"Pei Li,&nbsp;Zhen Yan","doi":"10.1016/j.ynstr.2023.100601","DOIUrl":"10.1016/j.ynstr.2023.100601","url":null,"abstract":"<div><p>Social isolation during adolescence can increase the risk of mental disorders. Epigenetic changes induced by chronic social isolation may serve as a mechanism underlying emotional disturbances. To test this, we exposed female mice to a post-weaning 6-week social isolation (SI) stress. We found the significantly increased methylation of histone H3 at lysine 9 (H3K9), a histone mark linked to gene repression, as well as the increased H3K9 methyltransferases SUV39H1 and SETDB1, in prefrontal cortex (PFC) of SI females. To find out potential downstream genes affected by this epigenetic alteration, we examined genes linked to neuronal and synaptic functions. Activity-dependent genes, including <em>Arc,</em> c<em>-Fos and Npas4,</em> were significantly reduced in PFC of SI females, correlated with the increased H3K9me2 occupancy around <em>Arc</em> enhancer. Treatment of SI females with UNC0642, a selective inhibitor of H3K9 methylation, significantly attenuated the anxiety-like behavior and elevated <em>Arc</em> expression. These results have revealed an epigenetic mechanism and intervention avenue for anxiety induced by chronic social isolation.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100601"},"PeriodicalIF":5.0,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289523000899/pdfft?md5=743463771afa274c9b60fa8c6ad2fc01&pid=1-s2.0-S2352289523000899-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138741990","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":"Subjective stress and any drinking during alcohol treatment: Disentangling within and between person autoregressive effects","authors":"Katie Witkiewitz ,&nbsp;Christian C. Garcia ,&nbsp;Bengt O. Muthén","doi":"10.1016/j.ynstr.2023.100602","DOIUrl":"10.1016/j.ynstr.2023.100602","url":null,"abstract":"<div><p>Alcohol use has been shown to increase stress, and there is some evidence that stress predicts subsequent alcohol use during treatment for alcohol use disorder (AUD), particularly among females who are more likely to report coping-motivated drinking. Gaining a better understanding of the processes by which stress and alcohol use are linked during treatment could potentially inform AUD treatment planning. The current study aimed to characterize the association between stress and drinking during the course of AUD treatment and whether there were sex differences in these associations. Secondary data analyses of the COMBINE study (N = 1375; 69% male, 76.3% non-Hispanic and white, average age of 44.4 years) were conducted to examine self-reported perceived stress and alcohol consumption across 16 weeks of treatment for AUD using a Bayesian random-intercept cross-lagged panel model. There was stronger evidence for any alcohol use predicting greater than typical stress in subsequent weeks and less strong evidence for stress increasing the subsequent probability of alcohol use, particularly among males. For females, greater stress predicted subsequent drinking earlier in the treatment period, and a lower probability of subsequent drinking in the last week of treatment. Interventions might specifically focus on targeting reductions in stress following drinking occasions.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100602"},"PeriodicalIF":5.0,"publicationDate":"2023-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289523000905/pdfft?md5=698995a43eb50ac178a15690581285e1&pid=1-s2.0-S2352289523000905-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138741925","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":"Theta oscillatory dynamics serving cognitive control index psychosocial distress in youth","authors":"Mikki Schantell ,&nbsp;Brittany K. Taylor ,&nbsp;Amirsalar Mansouri ,&nbsp;Yasra Arif ,&nbsp;Anna T. Coutant ,&nbsp;Danielle L. Rice ,&nbsp;Yu-Ping Wang ,&nbsp;Vince D. Calhoun ,&nbsp;Julia M. Stephen ,&nbsp;Tony W. Wilson","doi":"10.1016/j.ynstr.2023.100599","DOIUrl":"10.1016/j.ynstr.2023.100599","url":null,"abstract":"<div><h3>Background</h3><p>Psychosocial distress among youth is a major public health issue characterized by disruptions in cognitive control processing. Using the National Institute of Mental Health's Research Domain Criteria (RDoC) framework, we quantified multidimensional neural oscillatory markers of psychosocial distress serving cognitive control in youth.</p></div><div><h3>Methods</h3><p>The sample consisted of 39 peri-adolescent participants who completed the NIH Toolbox Emotion Battery (NIHTB-EB) and the Eriksen flanker task during magnetoencephalography (MEG). A psychosocial distress index was computed with exploratory factor analysis using assessments from the NIHTB-EB. MEG data were analyzed in the time-frequency domain and peak voxels from oscillatory maps depicting the neural cognitive interference effect were extracted for voxel time series analyses to identify spontaneous and oscillatory aberrations in dynamics serving cognitive control as a function of psychosocial distress. Further, we quantified the relationship between psychosocial distress and dynamic functional connectivity between regions supporting cognitive control.</p></div><div><h3>Results</h3><p>The continuous psychosocial distress index was strongly associated with validated measures of pediatric psychopathology. Theta-band neural cognitive interference was identified in the left dorsolateral prefrontal cortex (dlPFC) and middle cingulate cortex (MCC). Time series analyses of these regions indicated that greater psychosocial distress was associated with elevated spontaneous activity in both the dlPFC and MCC and blunted theta oscillations in the MCC. Finally, we found that stronger phase coherence between the dlPFC and MCC was associated with greater psychosocial distress.</p></div><div><h3>Conclusions</h3><p>Greater psychosocial distress was marked by alterations in spontaneous and oscillatory theta activity serving cognitive control, along with hyperconnectivity between the dlPFC and MCC.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"29 ","pages":"Article 100599"},"PeriodicalIF":5.0,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289523000875/pdfft?md5=9c4c77424401dc2b21cc10cc6a1ea270&pid=1-s2.0-S2352289523000875-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138684508","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":"Blue light at night produces stress-evoked heightened aggression by enhancing brain-derived neurotrophic factor in the basolateral amygdala","authors":"Zhenlong Li ,&nbsp;Chau-Shoun Lee ,&nbsp;Si Chen ,&nbsp;Benyu He ,&nbsp;Xinya Chen ,&nbsp;Hsien-Yu Peng ,&nbsp;Tzer-Bin Lin ,&nbsp;Ming-Chun Hsieh ,&nbsp;Cheng-Yuan Lai ,&nbsp;Dylan Chou","doi":"10.1016/j.ynstr.2023.100600","DOIUrl":"https://doi.org/10.1016/j.ynstr.2023.100600","url":null,"abstract":"<div><p>Light is an underappreciated mood manipulator. People are often exposed to electronic equipment, which results in nocturnal blue light exposure in modern society. Light pollution drastically shortens the night phase of the circadian rhythm. Preclinical and clinical studies have reported that nocturnal light exposure can influence mood, such as depressive-like phenotypes. However, the effects of blue light at night (BLAN) on other moods and how it alters mood remain unclear. Here, we explored the impact of BLAN on stress-provoked aggression in male Sprague‒Dawley rats, focusing on its influence on basolateral amygdala (BLA) activity. Resident-intruder tests, extracellular electrophysiological recordings, and enzyme-linked immunosorbent assays were performed. The results indicated that BLAN produces stress-induced heightened aggressive and anxiety-like phenotypes. Moreover, BLAN not only potentiates long-term potentiation and long-term depression in the BLA but also results in stress-induced elevation of brain-derived neurotrophic factor (BDNF), mature BDNF, and phosphorylation of tyrosine receptor kinase B expression in the BLA. Intra-BLA microinfusion of BDNF RNAi, BDNF neutralizing antibody, K252a, and rapamycin blocked stress-induced heightened aggressive behavior in BLAN rats. In addition, intra-BLA application of BDNF and 7,8-DHF caused stress-induced heightened aggressive behavior in naïve rats. Collectively, these results suggest that BLAN results in stress-evoked heightened aggressive phenotypes, which may work by enhancing BLA BDNF signaling and synaptic plasticity. This study reveals that nocturnal blue light exposure may have an impact on stress-provoked aggression. Moreover, this study provides novel insights into the BLA BDNF-dependent mechanism underlying the impact of the BLAN on mood.</p></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"28 ","pages":"Article 100600"},"PeriodicalIF":5.0,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352289523000887/pdfft?md5=3bc75819bd5857805476508414409697&pid=1-s2.0-S2352289523000887-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713250","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}