Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01569-6
Alexandra Le Bras
{"title":"Mapping the zebrafish regenerative heart","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01569-6","DOIUrl":"https://doi.org/10.1038/s41684-025-01569-6","url":null,"abstract":"<p>While adult mammals have an extremely limited capacity to repair lost or damaged heart tissue, many adult fish, including zebrafish, can successfully regenerate their hearts after injury. Uncovering the mechanisms of zebrafish heart regeneration could open new avenues to regenerate human hearts and prevent heart failure. In a new study, researchers combined the use of spatial transcriptomics (Stereo-seq) and single-cell RNA-sequencing (scRNA-seq) to generate a spatially-resolved molecular and cellular atlas of the regenerating zebrafish heart across eight stages, including pre-injury, 6 hours post-amputation (hpa) of the ventricular apex, 12 hpa, 1 day post-amputation (dpa), 3 dpa, 7 dpa, 14 dpa, and 28 dpa. Using this comprehensive atlas, they characterized the dynamic changes in cell type composition throughout cardiac regeneration, including proliferating macrophages, pro-regenerative fibroblasts and regenerating cardiomyocytes. The study also identified <i>tpm4a</i> as a critical gene for cardiomyocyte re-differentiation during the regeneration process. Finally, the researchers created a ‘virtual regenerating heart’, encompassing both spatial information and time, which can be accessed here: https://db.cngb.org/stomics/zebrafish_VRH/</p><p><b>Original reference:</b> Li, L. et al. <i>Nat. Commun</i>. <b>16</b>, 3716 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"260 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01565-w
Jorge Ferreira
{"title":"Prenatal infection impairs social communication","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01565-w","DOIUrl":"https://doi.org/10.1038/s41684-025-01565-w","url":null,"abstract":"<p>Sequencing deficits are considered a core feature of schizophrenia. A study in <i>Behavioral Brain Research</i> used the maternal immune activation (MIA) rat model—a model of increased neurodevelopmental disorder risk linked to prenatal infection—to investigate alterations in ultrasonic vocalization (USV) sequencing. While basic USV features remained intact, MIA rats exhibited significant disruptions in call sequence structure compared to control rats. Using USV sequence analysis with Markov chain analysis to study transition between vocalization types and Damerau-Levenshtein distance to study how different the sequences are across two datasets, researchers observed altered transition probabilities and reduced sequence similarity in MIA offspring compared to controls. These findings suggest that MIA selectively impairs higher-order vocal organization, linked to social communication, without affecting vocal production capacity. The results show the potential of using USV sequencing analysis as a preclinical behavioral marker of disrupted cognitive organization, relevant to schizophrenia. These results also reinforce the utility of the MIA model for studying sequence processing abnormalities in neuropsychiatric conditions.</p><p><b>Original reference:</b> Scott, K. J., Speers, L. J. and Bilkey, D. K. <i>Behav. Brain Res</i>. <b>488</b>, 115596 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"38 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01562-z
Jorge Ferreira
{"title":"Hippocampal microglia’s role in neuropathic pain","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01562-z","DOIUrl":"https://doi.org/10.1038/s41684-025-01562-z","url":null,"abstract":"<p>Neuropathic pain often occurs alongside cognitive impairment, but the mechanisms behind this relationship remain unclear. A study in <i>Behavioral Brain Research</i> investigates the microglial activation in brain regions involved in emotion, memory and pain processing in male mice of a partial sciatic nerve ligation (PSNL) model. Two weeks post-injury, Iba1 and P2RY12 immunoreactivity—two markers of microglial activation—were significantly increased in the hippocampus and amygdala, but not the perirhinal cortex. Targeted microinjection of clodronate liposomes, depleting microglia, into the hippocampus, but not the amygdala, alleviated both mechanical allodynia and cognitive deficits. Hippocampal clodronate treatment also prevented the PSNL-induced degenerative changes in neuronal morphology. These results show that hippocampal microglial activation has an important role in both pain sensitivity and cognitive dysfunction following nerve injury. The results support that region-specific microglial activation contributes to neuropathic pain and show that the hippocampus can be a potential therapeutic target.</p><p><b>Original reference:</b> Hisaoka-Nakashima, K. et al. <i>Behav. Brain Res</i>. <b>488</b>, 115590 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"41 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01566-9
Alexandra Le Bras
{"title":"Multigenerational effects of IVF","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01566-9","DOIUrl":"https://doi.org/10.1038/s41684-025-01566-9","url":null,"abstract":"<p>In vitro fertilization (IVF) is the most commonly used assisted reproductive technology to treat infertility. While most children conceived through IVF are healthy, some studies have observed potential long-term health effects, including a slightly higher risk of metabolic disorders. Previous studies in mice have also shown that IVF is associated with a higher risk of metabolic syndromes in offspring, confirming the suitability of mouse models for studying IVF and its potential adverse effects. According to a new study published in <i>JCI Insight</i>, IVF induces reproductive changes in male mouse offspring and has negative multigenerational effects. Compared to those conceived naturally, male offspring conceived via IVF exhibited decreased levels of testosterone, changes in testicular morphology, gene expression and DNA methylation, as well as changes in sperm morphology and DNA methylation. In addition, IVF-conceived males, when mated with wild-type females, sired F2 IVF offspring that exhibited altered metabolism compared to F2 naturally conceived offspring, including a higher risk of insulin and glucose resistance in males and a diabetic phenotype in females. These results highlight the need for continued research into the multigenerational effects of IVF.</p><p><b>Original reference:</b> Rhon-Calderon, E.A. et al<i>. JCI Insight</i>. <b>10,</b> e188931 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"17 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01567-8
Alexandra Le Bras
{"title":"Seasonal gene expression","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01567-8","DOIUrl":"https://doi.org/10.1038/s41684-025-01567-8","url":null,"abstract":"<p>To cope with the seasonal changes in the environment, many animal species exhibit seasonal variations in their physiology and behavior. Humans also show seasonal differences in various physiological processes, including those related to hormone secretion, metabolism, immune function and reproduction. To better understand the mechanisms underlying these seasonal changes, Chen and colleagues analyzed the seasonal transcriptome of samples of 80 tissues, including 30 brain regions and 50 peripheral tissues, collected over one year from male and female rhesus macaques (4- to 11-year-old) kept in a semi-natural outdoor environment. They identified seasonally oscillating genes (SOGs) in all tissues studied (273−2,344 SOGs in males vs. 342−1,943 SOGs in females), providing insights into the molecular basis of seasonally regulated physiology. The researchers also identified seasonal fluctuations in the expression of several disease-related genes, including the gene encoding serine protease TMPRSS2, which is used by SARS-CoV-2 to enter the cells. The data, which can be accessed in the Non-Human Primate Seasonal Transcriptome Atlas Database (NHPSTA) (https://rhythm.itbm.nagoya-u.ac.jp/NHPSTA/), could be a valuable resource to identify new therapies for seasonally regulated diseases.</p><p><b>Original reference:</b> Chen, J. et al<i>. Nat. Commun</i>. <b>16</b>, 3906 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"12 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01563-y
Jorge Ferreira
{"title":"Novel muscle injury treatment in rats","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01563-y","DOIUrl":"https://doi.org/10.1038/s41684-025-01563-y","url":null,"abstract":"<p>Muscle injuries are common in sports and daily life, involving inflammation, regeneration and remodeling of muscle tissue. A study in <i>Scientific Reports</i> evaluated the effects of two subtypes of platelet-rich plasma (PRP), the leukocyte-poor PRP (LP-PRP) and the leukocyte-rich PRP (LR-PRP), and the peptide antagonist of the domains 1 and 2 of the IL-1β receptor (DAP1-2) on inflammation following muscle contusion in Wistar rats. Treatment with LP-PRP and DAP1-2, individually or combined, showed the most significant effects. Notably, RT-qPCR and ELISA showed a modulation of early inflammation markers compared to the control injury group and that the treatment promotes an efficient transition from the initial inflammation stage to tissue regeneration. However, the study endpoint was five days post-injury, limiting insights into long-term effects. The combined use of LP-PRP and IL-1β inhibitor peptides may represent a novel therapeutic strategy for acute muscle injuries, but further research is needed to confirm efficacy and understand mechanisms of action.</p><p><b>Original reference:</b> Colares, M.C. et al. <i>Sci. Rep</i>. <b>15</b>, 14219 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"8 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01568-7
Alexandra Le Bras
{"title":"CAR T therapy affects mouse cognition","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01568-7","DOIUrl":"https://doi.org/10.1038/s41684-025-01568-7","url":null,"abstract":"<p>Many individuals experience cognitive impairment after cancer and cancer treatment. Patients have reported cancer-related cognitive impairment (CRCI) after traditional cancer treatments such as chemotherapy, radiation therapy and surgery, but also after immunotherapy. However, to date, the mechanisms driving CRCI in patients after immunotherapy are unclear. A new study shows that chimeric antigen receptor (CAR) T cell therapy causes cognitive impairment in mouse models of cancer by inducing neuroimmunological changes. In this study, the researchers used patient-derived xenograft murine models of both central nervous system (CNS) and non-CNS cancers, including a model of H3K27M-altered diffuse midline glioma, a pre-B cell acute lymphoblastic leukemia model, two osteosarcoma models and a melanoma model. Behavioral assessment revealed that treatment with CAR T cell therapy (targeting either GD2, CD19, or B7H3 according to tumor type) impaired cognitive performance compared to control mice treated with mock T cells. The treatment also induced neuroinflammation and persistent white matter microglial reactivity, with negative consequences on oligodendrocyte homeostasis and plasticity. These findings could guide the development of therapeutic interventions for patients living with persistent brain fog syndromes after immunotherapy.</p><p><b>Original reference:</b> Geraghty, A.C. et al. <i>Cell</i> https://doi.org/10.1016/j.cell.2025.03.041 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"31 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-03DOI: 10.1038/s41684-025-01564-x
Jorge Ferreira
{"title":"Fecal microbiota transplantation therapy","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01564-x","DOIUrl":"https://doi.org/10.1038/s41684-025-01564-x","url":null,"abstract":"<p>The gut microbiota influences both gastrointestinal and neurobehavioral health. A study in <i>Scientific Reports</i> investigated fecal microbiota transplantation (FMT) as a treatment for acetic acid-induced colitis and associated anxiety-like behaviors in rats. Colitis was induced via rectal acetic acid administration, leading to macroscopic colon damage, increased disease index, and elevated expression of NF-κB, NLRP3, Caspase1, IL-1β and IL-18, markers of inflammation, in colon and hippocampal tissues compared to untreated animals. FMT treatment significantly reduced acetic acid-induced colon pathology and suppressed the activation of the NLRP3-Caspase1 signaling pathway. Behavioral tests indicated that FMT also alleviated anxiety-like symptoms. Mechanistically, FMT downregulated NF-κB, NLRP3, and Caspase1 expression and decreased IL-1β and IL-18 levels in both the colon and hippocampus. These findings suggest that FMT exerts anti-inflammatory and anxiolytic effects through modulation of the NLRP3 inflammasome. FMT may serve as a therapeutic strategy for treating inflammatory bowel diseases and their associated neurobehavioral comorbidities.</p><p><b>Original reference:</b> Mohammadi, M. et al. <i>Sci. Rep</i>. <b>15</b>, 14831 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"38 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-01DOI: 10.1038/s41684-025-01570-z
Jorge Ferreira
{"title":"Factors contributing to the open-field test variability.","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01570-z","DOIUrl":"https://doi.org/10.1038/s41684-025-01570-z","url":null,"abstract":"","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"54 6","pages":"135"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-06-01DOI: 10.1038/s41684-025-01572-x
Alexandra Le Bras
{"title":"A new magnetic particle mouse model of stroke.","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01572-x","DOIUrl":"https://doi.org/10.1038/s41684-025-01572-x","url":null,"abstract":"","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"54 6","pages":"137"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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