Neurotoxicology and teratology最新文献

{"title":"Profiles of polysubstance exposure in youth with fetal alcohol spectrum disorders and the association with neurodevelopmental outcomes","authors":"Madeline N. Delage ,&nbsp;Emily L. Speybroeck ,&nbsp;Alesia A. Richardson ,&nbsp;Lynn L. Cole ,&nbsp;Carson Kautz-Turnbull ,&nbsp;Christie L.M. Petrenko","doi":"10.1016/j.ntt.2026.107585","DOIUrl":"10.1016/j.ntt.2026.107585","url":null,"abstract":"<div><h3>Background</h3><div>Prenatal polysubstance exposure is highly prevalent among individuals with fetal alcohol spectrum disorders (FASD), yet little research has examined how specific patterns of co-exposure relate to neuropsychological outcomes. While alcohol is a known teratogen, other substances such as opioids, stimulants, cannabis, and nicotine also disrupt neurodevelopmental processes. Prior studies often assess single substances in isolation, failing to reflect real-world exposure patterns. Identifying meaningful patterns of co-occurring exposures and their associations with neuropsychological outcomes is critical for advancing targeted assessment and intervention.</div></div><div><h3>Methods</h3><div>Latent class analysis was conducted on data from 635 youth with FASD (mean age of diagnosis 7.4 years, range 0.24–21.61) to identify distinct profiles of prenatal exposure to six substances: alcohol, nicotine, marijuana, opioids, cocaine, and other drugs. Class differences in neuropsychological functioning, postnatal experiences, and demographics were examined using the Bolck, Croon, and Hagenaars method.</div></div><div><h3>Results</h3><div>A three-class solution demonstrated best model fit (AIC = 3945.216, saBIC = 3970.790, aLRT = 18.521, <em>p</em> = .006). Classes comprised of an all-exposure (Class 1, 47%), mainly alcohol exposed (Class 2, 46%), and mainly opioid exposed (Class 3, 7%). Significant between-class differences emerged across domains of memory, motor speed, sensory processing, and child-reported anxiety (χ² = 9.264–42.659, <em>p</em> = .046–0.001). Class 2 demonstrated significantly greater neuropsychological challenges, while Class 3 demonstrated high sensory sensitivity and anxiety. Results also reveal caregiver disruption was more prevalent in Class 2.</div></div><div><h3>Discussion</h3><div>Findings highlight heterogeneity in neuropsychological outcomes based on distinct patterns of prenatal polysubstance exposures. Neuropsychological assessment remains essential for capturing this variability and informing individualized, exposure-responsive care.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"114 ","pages":"Article 107585"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146102581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental factors associated with microcephaly in Africa: A systematic review","authors":"Pelagie Izabayo ,&nbsp;Jean Claude Hakizimana ,&nbsp;Annette Uwineza ,&nbsp;Abdullateef Isiaka Alagbonsi","doi":"10.1016/j.ntt.2025.107577","DOIUrl":"10.1016/j.ntt.2025.107577","url":null,"abstract":"<div><h3>Introduction</h3><div>Microcephaly, a condition characterized by a head circumference below the mean for age and sex, is a significant indicator of impaired fetal brain development. While some environmental factors have been associated with the development of microcephaly in Africa, the available information remains disjointed, making it difficult for healthcare providers and policy makers to translate the information to preventive measures in maternal and child health. This systematic review aims to synthesize primary studies on environmental determinants of microcephaly, focusing on African populations.</div></div><div><h3>Method</h3><div>A systematic literature search was conducted using PubMed, Scopus, AJOL, and Wiley Online Library to identify studies published between 2000 and 2025, focusing on environmental exposures and microcephaly in neonates and infants. Observational and interventional studies in English were included, following PRISMA 2020 guidelines. Data were extracted and tabulated by country, exposure type, study design, and reported outcomes.</div></div><div><h3>Results</h3><div>Sixteen African studies found a multifactorial relationship between environmental exposures and microcephaly. Zika virus infection was a consistent contributor, with maternal febrile illnesses, inadequate antenatal care, HIV exposure, and heavy metal toxicity also linked. Pesticide exposure, particularly to organophosphates and DDT, was associated with neurodevelopmental delays and restricted cranial growth. Ambient air pollution was negatively correlated with neonatal head circumference. Socioeconomic vulnerabilities intensified these environmental risks, especially during epidemic crises like Zika virus outbreaks.</div></div><div><h3>Conclusion</h3><div>Microcephaly in African populations is a multifactorial issue, influenced by emerging infections like ZIKV, chronic environmental exposures, and healthcare gaps. It calls for integrated public health strategies, including surveillance, early prenatal screening, environmental regulation, and region-specific diagnostic standards. Global evidence supports shared biological vulnerability in low-resource settings.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"113 ","pages":"Article 107577"},"PeriodicalIF":2.8,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational and early childhood air pollution exposure and neurodevelopmental outcomes in early childhood","authors":"Christina Berninger ,&nbsp;Yingying Xu ,&nbsp;Patrick Ryan ,&nbsp;Kim M. Cecil ,&nbsp;Bruce P. Lanphear ,&nbsp;Aimée Vester ,&nbsp;Kimberly Yolton","doi":"10.1016/j.ntt.2025.107576","DOIUrl":"10.1016/j.ntt.2025.107576","url":null,"abstract":"<div><h3>Background</h3><div>Exposure to ambient air pollution, including fine particulate matter (PM_2.5), nitrogen dioxide (NO₂), and elemental carbon, has been associated with worse neurodevelopmental outcomes in children, but research on early childhood outcomes is limited.</div></div><div><h3>Objective</h3><div>This study examined the associations between gestational and early childhood exposures to PM_2.5 and NO₂ and child developmental outcomes measured at ages 1, 2, and 3 years.</div></div><div><h3>Methods</h3><div>In the Health Outcomes and Measures of the Environment (HOME) Study, a longitudinal pregnancy and birth cohort, we used spatiotemporal models to estimate the concentration of each air pollutant at participants' home addresses during early brain development. Neurodevelopmental outcomes were measured using the Bayley Scales of Infant Development, Second Edition (BSID-II) at ages 1, 2, and 3 years. For 329 children, we examined the associations of air pollution with BSID-II scores using generalized linear models with generalized estimating equations (GEE).</div></div><div><h3>Results</h3><div>Gestational and early childhood NO₂ concentrations were positively associated with cognitive development at age 1 year but negatively associated with cognitive development at age 3 years. Similarly, PM_2.5 exposure through age 3 years was negatively associated with cognitive development at age 3 years. Gestational NO₂ concentration was positively associated with motor development at age 1 year but negatively associated with motor development at ages 2 and 3 years.</div></div><div><h3>Discussion</h3><div>These results suggest that exposure to traffic-related air pollution during gestation and after birth may impact neurodevelopment in early childhood.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"113 ","pages":"Article 107576"},"PeriodicalIF":2.8,"publicationDate":"2025-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is there a glymphatic pathway to environmental risk in neurodevelopmental disorders?","authors":"Maiara de Aguiar da Costa ,&nbsp;Sofia Januário Bolan ,&nbsp;Maria Fernanda Pedro Ebs ,&nbsp;Simone Lespinasse Araújo ,&nbsp;Cristiano Juliano Faller ,&nbsp;Tatiana Barichello ,&nbsp;Michael Aschner ,&nbsp;Jaqueline da Silva Generoso ,&nbsp;Cinara Ludvig Gonçalves","doi":"10.1016/j.ntt.2025.107578","DOIUrl":"10.1016/j.ntt.2025.107578","url":null,"abstract":"<div><div>The glymphatic system (GS) is a glia-dependent perivascular network that mediates cerebrospinal fluid-interstitial fluid exchange and facilitates the clearance of neurometabolites. GS transport is sleep-dependent, with waste elimination heightened during non-rapid eye movement sleep. Emerging evidence links GS dysfunction with neurodevelopmental disorders (NDDs), including autism spectrum disorder, schizophrenia, and attention-deficit/hyperactivity disorder, disorders that frequently co-occur with sleep disturbances. In parallel, multiple environmental toxicants have been associated with adverse neurodevelopment. This study aims to integrate current evidence on the interplay between toxicants, GS dysfunction, and NDDs, highlighting shared biological pathways and exploring potential therapeutic targets. Evidence gaps include the absence of studies directly investigating toxicant effects on GS within NDDs populations, limited longitudinal data across sensitive developmental windows, scarce integration of GS-sensitive imaging, cerebrospinal fuid (CSF) biomarkers, and underassessment of sex differences and exposure mixtures. Translational opportunities span sleep optimization and GS-targeted strategies (e.g., enhancing CSF transport); among pharmacologic candidates, the α2-adrenergic agonist dexmedetomidine shows sedative–anxiolytic, anti-inflammatory, and neuroprotective signals warranting investigation. This narrative review synthesizes current evidence and delineates priorities to test the exposome–glymphatic–neurodevelopment axis.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"113 ","pages":"Article 107578"},"PeriodicalIF":2.8,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145743465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprogramming of prenatal phthalate exposures on fluid cognition: A latent variable modeling approach to quantify exposure burden and integrate neurobehavioral data","authors":"Jamil M. Lane ,&nbsp;Nathan Cohen ,&nbsp;Vishal Midya ,&nbsp;Cecilia S. Alcala ,&nbsp;Shoshannah Eggers ,&nbsp;Sandra Martinez-Medina ,&nbsp;Damaskini Valvi ,&nbsp;Martha M. Téllez-Rojo ,&nbsp;Deborah A. Cory-Slechta ,&nbsp;Robert O. Wright ,&nbsp;Shelley H. Liu","doi":"10.1016/j.ntt.2025.107575","DOIUrl":"10.1016/j.ntt.2025.107575","url":null,"abstract":"<div><h3>Background</h3><div>Phthalates are endocrine-disrupting chemicals with neuroactive properties linked to maladaptive neurodevelopment in children. However, few studies have utilized latent variable methodologies to estimate their cumulative impact and assess the complex integration of cognitive processes that characterize fluid cognition—the ability to efficiently process, manipulate, and integrate information to solve reasoning problems.</div></div><div><h3>Objective</h3><div>We investigated the prenatal trimester-specific neuroprogramming effects of the phthalate burden scores on fluid cognition in Mexican children.</div></div><div><h3>Methods</h3><div>Children (<em>n</em> = 626) aged 6–7 years from a prospective pregnancy cohort in Mexico City were administered subtests from the CANTAB, completing the between error, strategy, and mean latency measures intended to evaluate a broad spectrum of cognitive domains representative of fluid cognition. Phthalate metabolites were measured in maternal urine collected at 2nd and 3rd pregnancy trimesters. A CFA validated and quantified two correlated latent phthalate burden scores representing prenatal exposure to low molecular weight (LMW) and high molecular weight (HMW) phthalates. Trimester-specific models using a covariate-adjusted SEM estimated the associations of latent phthalate burden scores with a latent construct of fluid cognition, an integration of working memory, executive function, and attention tasks.</div></div><div><h3>Results</h3><div>In the 3rd trimester, higher LMW phthalate burden was associated with poorer fluid cognition (b = −1.860; [95 % CI = −3.505, −0.215]; <em>p</em> = 0.027), while HMW phthalate burden showed a positive association (b = 1.815; [95 % CI = 0.176, 3.453]; <em>p</em> = 0.030). Conversely, in the 2nd trimester, neither burden levels of LMW (b = −0.508; [95 % CI = −1.639, 0.623]; <em>p</em> = 0.378) nor HMW (b = 0.451; [95 % CI = −0.671, 1.573]; <em>p</em> = 0.431]; <em>p</em> = 0.44) phthalate demonstrated significant associations with fluid cognitive performance.</div></div><div><h3>Conclusion</h3><div>The temporal sensitivity of prenatal phthalate exposures on fluid cognition showed effects in later stages, with higher LMW burden linked to poorer performance and HMW burden showing a positive association. Our findings emphasize latent variable approaches and the need for more research on exposure-driven integrated cognitive programming.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"113 ","pages":"Article 107575"},"PeriodicalIF":2.8,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sevoflurane induced hippocampal neuron cell injury via the miR-132-5p/BDNF axis and further caused cognitive impairment in rats","authors":"Junbo Peng ,&nbsp;Xiaoxiao Dai ,&nbsp;Guohai Chu","doi":"10.1016/j.ntt.2025.107567","DOIUrl":"10.1016/j.ntt.2025.107567","url":null,"abstract":"<div><h3>Background</h3><div>Sevoflurane (Sevo) could cause cognitive dysfunction in patients. MiR-132-5p is associated with nervous system functions. Therefore, this study explored the role of miR-132-5p in Sevo-induced cognitive impairment. This study aimed to provide useful information on preventing Sevo-induced cognitive impairment.</div></div><div><h3>Methods</h3><div>Sprague-Dawley rats and HT22 cells were involved in this study. A Sevo-treated rat model was constructed by making the rat inhale 2 % Sevo for 5 h. A Morris water maze (MWM) assay was conducted to assess the cognitive ability of rats. The qRT-PCR was used to measure miRNA and gene expression. Western Blot was used to measure protein expression. The oxidative stress status was measured using antioxidant activity assay. The flow cytometry was applied for the cell apoptosis assay. The mechanism was investigated using dual luciferase reporter assay.</div></div><div><h3>Results</h3><div>Sevo impaired the cognitive function of rats. Sevo-treatment upregulated miR-132-5p in rat hippocampal tissues, and miR-132-5p further downregulated BDNF. MiR-132-5p mediated the effect of Sevo on rat cognitive functions. MiR-132-5p affected rat cognitive functions by downregulating BDNF. In hippocampal neuron cells, Sevo-treatment upregulated miR-132-5p, and miR-132-5p downregulated BDNF. MiR-132-5p mediated the disrupting effect of Sevo on hippocampal neuron cells. MiR-132-5p caused hippocampal neuron cell damage by downregulating BDNF.</div></div><div><h3>Conclusion</h3><div>Sevo could induce rat cognitive impairments. Sevo-treatment upregulated miR-132-5p and miR-132-5p could downregulate BDNF expression in hippocampal tissues and neuron cells. MiR-132-5p mediated the disrupting effect of Sevo on hippocampal neuron cells and cognitive functions. MiR-132-5p caused hippocampal neuron cell injury and cognitive dysfunction by downregulating BDNF.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107567"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145391693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction to developmental outcomes of neuroinflammatory insults","authors":"Laura M. Carlson ,&nbsp;G. Jean Harry ,&nbsp;Kelly Carstens","doi":"10.1016/j.ntt.2025.107566","DOIUrl":"10.1016/j.ntt.2025.107566","url":null,"abstract":"","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107566"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145459216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodevelopmental effects of exogenous cannabinoids on endocannabinoid and GABAergic neurotransmission","authors":"Miles T. Wiley ,&nbsp;Adrian H. Courville ,&nbsp;Hayden Northcutt ,&nbsp;Iva Durdanovic ,&nbsp;Kawsar U. Chowdhury ,&nbsp;Vishnu Suppiramaniam ,&nbsp;Miranda N. Reed","doi":"10.1016/j.ntt.2025.107568","DOIUrl":"10.1016/j.ntt.2025.107568","url":null,"abstract":"<div><div>Cannabis is the most widely used illicit drug among pregnant women, and its use has been linked to higher risks of hyperactivity, attention issues, anxiety, depression, and reduced cognitive abilities in children. Cannabinoids cross the placenta and affect the fetal endocannabinoid (eCB) system, which is crucial for neurodevelopment and interacts with other key neurotransmitter systems, such as GABA, that regulate the proliferation, migration, differentiation, and plasticity of developing neurons. This review discusses the effects of exogenous cannabinoids on the eCB and GABAergic systems during neurodevelopment, including recent findings that exposure to exogenous cannabinoids can delay the developmental transition of GABA from a depolarizing to a hyperpolarizing state. This paper also examines the consequences of delayed GABA switching during early postnatal development and considers its potential long-term effects on brain function. These findings expand our understanding of maternal cannabis use and highlight the need for further research to clarify mechanisms, identify potential treatment targets, and evaluate public health impacts as cannabis use during pregnancy rises.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107568"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145573987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal corticosteroid use and offspring neurological outcomes","authors":"Yun Yan ,&nbsp;Junyi Wang ,&nbsp;Xiaoping Lei","doi":"10.1016/j.ntt.2025.107564","DOIUrl":"10.1016/j.ntt.2025.107564","url":null,"abstract":"<div><div>Prenatal use of synthetic corticosteroids has been widely applied in preventing respiratory distress syndrome in preterm infants. In recent years, research has begun to focus on the effects of Antenatal Corticosteroids(ACS) on the short-term and long-term neurological development of offspring. This review summarizes the direct and potential effects of ACS on offspring neurological outcomes, including cognitive function, behavioral problems, and neurodevelopmental disorders. Studies have shown that prenatal corticosteroid exposure may be associated with improved short-term neurological outcomes in extremely preterm infants. However, the benefits on near- and long-term outcomes in late preterm and full-term infants remain inconclusive and controversial due to a lack of robust evidence. This article explores the potential effects of exposure timing and different dosages on offspring neurological outcomes, and emphasizes the need for further research to optimize the indications for ACS use. This will ensure its benefits in preterm complications while minimizing its potential negative impact on offspring neurodevelopment.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107564"},"PeriodicalIF":2.8,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential cognitive, behavioral, and neurochemical responses to acute chlorpyrifos exposure in normotensive compared to hypertensive adult rats","authors":"Gabriel Gavazza Noé ,&nbsp;Larissa de Jesus Corrêa ,&nbsp;Janne Ketly da Silva Oliveira ,&nbsp;Karoline de Oliveira Sant'Anna ,&nbsp;Vitor Sampaio Minassa ,&nbsp;Andrew Vieira Aitken ,&nbsp;Karla Nivea Sampaio ,&nbsp;Vanessa Beijamini","doi":"10.1016/j.ntt.2025.107565","DOIUrl":"10.1016/j.ntt.2025.107565","url":null,"abstract":"<div><div>Clinical and preclinical evidence points to a bilateral association between cardiovascular diseases (CVD) and mental disorders such as anxiety and depression. We previously reported that exposure to organophosphate (OP) compounds, such as chlorpyrifos (CPF), promotes cardiovascular damage and behavioral alterations in normotensive rats. Also, spontaneously hypertensive rats (SHR), a well-established rodent model of hypertension, exhibit more severe symptoms of acute CPF toxicosis and higher mortality rates, likely due to lower plasma butyrylcholinesterase (BuChE) activity. The potential role of pre-existing hypertension in increasing susceptibility to acute OP toxicity, particularly in relation to psychiatric disorders, remains an open question. Given this, we investigated whether SHR are more susceptible than normotensive Wistar rats to the damage caused by acute CPF exposure on innate (elevated plus maze, EPM; light-dark transition, LDT; and open field tests) and learned (contextual fear conditioning) anxiety-like behaviors. A single dose of CPF (20 mg/kg) induced an anxiolytic-like behavior in SHR exposed to the EPM and no effect in Wistar rats. CPF acute intoxication increased fear expression in both strains, but impaired memory extinction only in Wistar rats. CPF inhibited BuChE in Wistar at all tested doses (10, 20 and 30 mg/kg), whereas inhibition occurred only at the highest dose in SHR. CPF also decreased acetylcholinesterase (AChE) activity in the hippocampus and prefrontal cortex of both strains. In summary, acute intoxication with CPF induces strain-dependent behavioral changes. SHRs intoxicated with CPF may not be the most suitable model for studying anxiety susceptibility to OP intoxication in previously hypertensive rats.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107565"},"PeriodicalIF":2.8,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}