International Journal of Developmental Neuroscience最新文献

{"title":"Music Aggravates Catechol-Induced Behavioural Abnormality and Redox Imbalance in Zebrafish","authors":"Yaqian Xiao,&nbsp;Dechang Rong,&nbsp;Hongjia Ye,&nbsp;Yifan Duan,&nbsp;Lichen Qiao,&nbsp;Lanlan Zuo,&nbsp;Lingtong Liu,&nbsp;Hasan Bayram,&nbsp;Jun Wang","doi":"10.1002/jdn.70018","DOIUrl":"https://doi.org/10.1002/jdn.70018","url":null,"abstract":"<div>\u0000 \u0000 <p>Catechol, also known as pyrocatechol, is a widespread antioxidant carcinogen that has been shown to cause central nervous system damage and metabolic abnormalities, and in zebrafish, it has been shown that exposure to aqueous solutions of catechol results in reduced pigmentation and decreased basal locomotor rate in juvenile zebrafish. However, the effects of catechol on zebrafish redox and behaviour are unknown. The aim of this study was to investigate the effects of catechol on oxidative stress levels in early zebrafish development and on behaviour in later stages of zebrafish development and to attempt to intervene in this effect with music therapy. We exposed zebrafish adults and juveniles to catechol separately, tested zebrafish juveniles for various redox indices and found that zebrafish juveniles had increased levels of reactive oxygen species and decreased total antioxidant capacity and lipid peroxidation capacity, and we tested zebrafish adults for behavioural studies and found that anxiety behaviours increased as social cohesion decreased. We then conducted a music therapy intervention for catechol exposure in adult zebrafish and found that music therapy exacerbated catechol-induced behavioural abnormalities and altered oxidative levels, whether zebrafish were exposed to both catechol and classical music or whether the catechol exposure was followed by a 12-day classical music intervention after 12 days of catechol exposure. In summary, this study revealed for the first time that catechol caused redox imbalance in juvenile zebrafish and socially disturbed, anxious behaviour in adults and found that music treatment worsened this behavioural abnormality. This study provides new insights into the effects of catechol on zebrafish and suggests that the therapeutic effects of music therapy may have a double-edged effect.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small SNPs, Big Effects: A Review of Single Nucleotide Variations and Polymorphisms in Key Genes Associated With Autism Spectrum Disorder","authors":"Sriharikrishnaa Srinath,&nbsp;Akanksha Kalal,&nbsp;Preethika Anand,&nbsp;Satyajit Mohapatra,&nbsp;Prabahan Chakraborty","doi":"10.1002/jdn.70016","DOIUrl":"https://doi.org/10.1002/jdn.70016","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterised by significant genetic variation. This article examines genetic alterations linked to ASD, with a specific emphasis on single nucleotide polymorphisms (SNPs) and single nucleotide variants (SNVs). Recent genome-wide association studies (GWAS) have identified several genetic variations associated with ASD. Although their precise roles remain unclear, such genetic polymorphisms and variations significantly influence several neurodevelopmental processes. Mutations in <i>SHANK3</i> and <i>NRXN1</i>, for example, disrupt synaptic activity and neurotransmission, contributing to ASD and intellectual deficits. Similarly, <i>PTEN</i> and <i>MECP2</i>, crucial for brain development, are associated with abnormal cell proliferation and neurodevelopmental disorders when mutated. <i>CHD8</i>, a key regulator of chromatin remodelling, is strongly linked to ASD, with its mutations impacting transcriptional regulation and neurodevelopment, while mutations in <i>SCN2A</i> disrupt neuronal excitability and synaptic transmission. In this review, we discuss SNPs and SNVs across these six key genes, to summarise their impact on the aetiology of ASD. A shift of focus in autism genetics giving equal importance to minor variations is critical to better understand the intricate aetiology of ASD and to create specific treatment strategies.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Orexin-A, Adiponectin and Apelin-13 Serum Levels in Children Diagnosed With Attention Deficit Hyperactivity Disorder","authors":"Serdar Avunduk,&nbsp;Ömer Başay,&nbsp;Süleyman Demir,&nbsp;Ayşen Çetin Kardeşler","doi":"10.1002/jdn.70014","DOIUrl":"https://doi.org/10.1002/jdn.70014","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigates the role of orexin-a, adiponectin (HMWA) and apelin-13 serum levels in the etiopathogenesis of attention deficit hyperactivity disorder (ADHD), a neurodevelopmental disorder with unclear aetiology involving neuropathological, genetic and environmental factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study involved 37 children with ADHD and 35 healthy controls, aged 6–18 years, with no history of other physical or psychiatric illnesses and no psychotropic medication use in the last 6 months. Serum levels of orexin-a, adiponectin (HMWA) and apelin-13 were measured using enzyme-linked immunosorbent assay (ELISA). ADHD symptoms were assessed through Diagnostic and Statistical Manual of Mental Disorders-5 (DSM-5)–based clinical interviews, Conners Parent and Teacher Rating Scales and Wisconsin Card Sorting Test.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>No significant differences in serum orexin-a, adiponectin (HMWA) and apelin-13 levels were found between the ADHD and control groups. Additionally, there was no relationship between orexin-a, apelin-13 and adinopectin levels and ADHD symptoms and Wisconsin Card Sorting Test results. Analysis of adiponectin levels in preadolescent children aged 6–11, adjusting for age and BMI, revealed a statistically significant reduction in the ADHD group (<i>p</i> = 0.002).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The results did not demonstrate any correlation between ADHD and the levels of orexin-a and apelin-13. However, the study revealed that children with ADHD, aged 6–11, exhibited decreased adiponectin concentrations. These results suggest that a decrease in serum adinopectin levels may be associated with ADHD in children.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143726835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinal Nerve Fibre Layer Thickness, Maküler Thickness and Macular Volume in Children With Intellectual Disability","authors":"Umut Karaaslan,&nbsp;Hatice Altun,&nbsp;Ayşegül Çömez","doi":"10.1002/jdn.70013","DOIUrl":"https://doi.org/10.1002/jdn.70013","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>It was aimed to investigate retinal nerve fibre layer (RNFL) thickness, macular thickness and macular volume and the relationship between these parameters and the Weschler Intelligence Scale for Children (WISC-R) in children with intellectual disability (ID).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study included 41 (27 male and 14 female) patients of ages 7–18 who were diagnosed with ID and 41 age- and sex-matched healthy individuals (24 male and 17 female). WISC-R intelligence test was applied with all the participants, and the parents were asked to fill out a Sociodemographic Data Form and the Strengths and Difficulties Questionnaire (SDQ). The RNFL, macular thickness and macular volume were examined by optical coherence tomography (OCT).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The RNFL was lower in all the quadrants (nasal, temporal, superior and inferior) in the patient group, but this thinness was not statistically significant in comparison to the control group. The left eye central macular and lest eye mean macular thicknesses were significantly lower in the patient group (respectively, <i>p</i> = 0.030, <i>p</i> = 0.048). Though not statistically significant, other all macular thickness and volume values were lower in the patient group in comparison to the control group. In the patient group, a weak negative correlation was observed between the performance subscore of the WISC-R and the RNFL values of the right eye inferior quadrant, as well as the left eye inferior and temporal quadrants (respectively, <i>r</i> = −0.329, <i>p</i> = 0.036; <i>r</i> = −0.308, <i>p</i> = 0.050; <i>r</i> = −0.309, <i>p</i> = 0.050). Additionally, a weak negative correlation was found between the total WISC-R scores and the RNFL values of the left eye temporal quadrant (<i>r</i> = −0.318, <i>p</i> = 0.043).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study suggests that macular thickness are reduced in ID patients but show no statistically significant changes in the RNFL. Lower macular thickness may potentially be linked to the brain abnormalities seen in ID, given the shared developmental origin of the retina and central nervous system. Further studies are needed to determine the potential application of OCT as a tool for diagnosing and monitoring the progression of this disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Agmatine Ameliorates Valproic Acid-Induced Depletion of Parvalbumin-Positive Neuron’","authors":"","doi":"10.1002/jdn.70015","DOIUrl":"https://doi.org/10.1002/jdn.70015","url":null,"abstract":"<p>\u0000 <span>Khoram-Abadi, K. M.</span>, <span>Basiri, M.</span>, <span>Nemati, M.</span>, &amp; <span>Nozari, M.</span> (<span>2024</span>). <span>Agmatine ameliorates valproic acid-induced depletion of parvalbumin-positive neuron</span>. <i>International Journal of Developmental Neuroscience</i>, <span>84</span>(<span>2</span>), <span>134</span>–<span>142</span>. https://doi.org/10.1002/jdn.10314.\u0000 </p><p>Figures 2, 3 and 4 unexpectedly contain similar images across the different experimental groups. The authors may have unintentionally mixed them up, and mistakes could have occurred during the figure assembly process.</p><p>The correct figures are provided below:</p><p>The authors apologise for any inconvenience this error may have caused.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jdn.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel KMT2E Splicing Variant as a Cause of O'Donnell–Luria–Rodan Syndrome With West Syndrome: Expansion of the Phenotype and Genotype","authors":"Qianyun Cai,&nbsp;Fan Feng,&nbsp;Haijiao Wang,&nbsp;Yanmei Tian,&nbsp;Rong Luo,&nbsp;Fan Yang,&nbsp;Xiao Qian,&nbsp;Zhongjie Zhou","doi":"10.1002/jdn.70012","DOIUrl":"https://doi.org/10.1002/jdn.70012","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>O'Donnell–Luria–Rodan (ODLURO) syndrome is an autosomal dominant disorder associated with <i>KMT2E</i> gene variants. ODLURO syndrome is characterized mainly by developmental delay, intellectual disability and macrocephaly or microcephaly; in some patients, it may manifest as autism or epilepsy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Trio whole-exome sequencing was performed on a female infant with unexplained West syndrome and developmental regression. A de novo splicing variant in the <i>KMT2E</i> gene was identified. The effects of this variant were analysed via a minigene splice assay and in vitro reverse transcription PCR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The patient presented with spasmodic seizures and developmental delay at 6 months of age. The video electroencephalogram (EEG) displayed hypsarrhythmia. Brain MRI revealed abnormal signals around the lateral ventricles and decreased white matter volume. A novel splicing variant in the <i>KMT2E</i> gene (NM_182931.3: c.1248_1248+9del) was identified in our proband. Sanger sequencing confirmed that the variant was not inherited from her parents. The in vitro minigene assay confirmed that c.1248_1248+9del resulted in exon 12 skipping.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>To our knowledge, this is the first definite report of ODLURO syndrome with West syndrome as the original manifestation. The deleterious effects of <i>KMT2E</i> c.1248_1248+9del were demonstrated in our proband. Splicing variants in the <i>KMT2E</i> gene are rare, and our study expands the phenotype and genotype of ODLURO syndrome. Additional studies are needed to explore the genotype–phenotype correlations of this disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of Empathy-Like Behaviour in Valproic Acid–Induced Rat Model of Autism","authors":"Süeda Tunçak,&nbsp;Bülent Gören,&nbsp;Tayfun Uzbay,&nbsp;Pınar Öz","doi":"10.1002/jdn.70008","DOIUrl":"https://doi.org/10.1002/jdn.70008","url":null,"abstract":"<div>\u0000 \u0000 <p>Prenatal VPA exposure is used to model ASD-like symptoms. Disrupted empathy is frequently observed in individuals with ASD, but empathy-like behaviour is not well documented in animal models. Pregnant Wistar Albino rats were administered either 400 mg/kg VPA or saline i.p. on E12.5. Empathy-like behaviour was assessed at P30 and P60 in both female and male offspring, who were also tested for olfactory discrimination, sociability, locomotor activity, and pre-pulse inhibition. Prenatal exposure to VPA significantly impaired empathy-like behaviour, as measured by the duration of time the subject spent with its sibling and the frequency of attempts to open the restrainer door. When P30 and P60 results were compared within groups, a developmental arrest in empathy-like behaviour was observed in the VPA group, whereas the control group showed improvement in their scores. Prenatal exposure to VPA also resulted in significantly decreased sociability and pre-pulse inhibition rates. In this study, an adapted version for measuring empathy-like behaviour has been proposed. This version involved a restrained sibling and no prior training, allowing the measurement to be independent of learning, memory, and stranger anxiety. The results show that VPA has negative effects on social development and is a valid tool for modelling ASD in both females and males.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Investigation of Neuronal–Astroglial Injury Proteins and MMP-9 Serum Levels in Autism Spectrum Disorder and Their Relationship With Autistic Regression","authors":"","doi":"10.1002/jdn.70011","DOIUrl":"https://doi.org/10.1002/jdn.70011","url":null,"abstract":"<p>\u0000 <span>Devecioğlu, H.</span>, <span>Tan, Ç.</span>, <span>Mısır, E.</span>, <span>Esen, H.</span>, <span>Özbek, B.</span> and <span>Kültür, S.</span> (<span>2025</span>), <span>Investigation of Neuronal–Astroglial Injury Proteins and MMP-9 Serum Levels in Autism Spectrum Disorder and Their Relationship With Autistic Regression</span>. <i>International Journal of Developmental Neuroscience</i>, <span>85</span>: e70005. https://doi.org/10.1002/jdn.70005.\u0000 </p><p>The department of one of the authors, Sadriye Ebru Çengel Kültür, has been incorrectly stated. It should be ‘Faculty of Medicine, Department of Child and Adolescent Psychiatry, Hacettepe University, Ankara, Turkey’.</p><p>We apologize for this error.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 2","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jdn.70011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Valproic Acid and Maternal Deprivation on Autism-Like Behaviours and Neurodevelopmental Outcomes in Female and Male Rats","authors":"Sara Sheibani Tezerji,&nbsp;Hossein Jonaidi,&nbsp;Vahid Sheibani,&nbsp;Amirhossein Moslemizadeh,&nbsp;Shahrzad Azizi,&nbsp;Maryam Dalili,&nbsp;Hamideh Bashiri,&nbsp;Sedigheh Amiresmaili","doi":"10.1002/jdn.70004","DOIUrl":"https://doi.org/10.1002/jdn.70004","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by persistent social communication deficits and restricted, repetitive behaviours, with significant overlap in anxiety-related symptoms. Both genetic and environmental factors contribute to the development of ASD, with early-life stressors, such as maternal separation (MS), and exposure to neurotoxic agents, like valproic acid (VPA), being key environmental contributors. This study investigates the combined impact of maternal deprivation (MD) and postnatal VPA exposure on autism-like behaviours and neurodevelopmental outcomes in male and female rats. Rats exposed to MD from postnatal days 2 to 4 exhibited significant changes in social interaction and anxiety-like behaviours, with female rats being more sensitive to MD than males. Postnatal VPA exposure resulted in similar behavioural alterations, including increased anxiety and social impairment, aligning with previous findings of VPA-induced neurodevelopmental deficits. A combination of MD and VPA exposure exacerbated anxiety-like behaviours in females, indicating that early-life stress and environmental toxins can synergistically affect neurodevelopment. Our results further suggest that the impact of these exposures may differ between sexes, with females showing heightened sensitivity to both MD and VPA-induced stress. These findings provide valuable insights into the complex interactions between genetic, environmental and epigenetic factors in ASD pathophysiology. The study underscores the critical role of early-life stressors, such as MD, in exacerbating neurodevelopmental disorders, particularly when combined with neurotoxic environmental factors like VPA. The sex-specific differences observed in behavioural outcomes suggest the importance of considering biological sex in future ASD research and therapeutic strategies.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Evaluation of Neuronal PARP-1 and Caspase-3 Levels in the Brain Tissue of Female Rats Exposed to Electromagnetic Fields at Different Gestational Stages","authors":"Kıymet Kübra Tüfekci,&nbsp;Musa Tatar,&nbsp;Abdalla Ahmed Eldaw Elamin,&nbsp;Süleyman Kaplan","doi":"10.1002/jdn.70010","DOIUrl":"https://doi.org/10.1002/jdn.70010","url":null,"abstract":"<div>\u0000 \u0000 <p>Foetal exposure to electromagnetic fields (EMFs) may cause marked neurocognitive impairment, although the mechanisms involved are still unclear. EMF induces region-specific neuronal and astroglial death in the rat hippocampus. Poly (ADP-ribose) polymerase-1 (PARP-1) regulates necrosis, apoptosis and other cellular processes occurring following injury. This study, therefore, investigated whether PARP-1 also regulates neuronal responses in the hippocampus of rats subjected to EMF radiation during different developmental periods. Male and female rats were first allowed to mate in separate cages. Rats identified as pregnant were then divided into four groups. A 900-MHz EMF was applied for 2 h daily on gestational days (GD) 1–7, GD 8–14 and GD 15–21. The female offspring were sacrificed at the end of the 28th postnatal day, and PARP-1 and Caspase-3 expressions in the hippocampus were then evaluated. No special treatment was applied to the control group. In the EMF-exposed group, pyramidal neurons in the cornu ammonis (CA) region appeared normal after exposure on GD 1–7 but were darkly stained and shrunken after exposure on GD 15–21, while the majority of granular cells exhibited a normal appearance during all GDs. The group exposed to EMF on GD 15–21 exhibited strong PARP-1 and Caspase-3 immune reactivity in CA and dentate gyrus (DG) cells. Higher H-scores were also observed in the EMF-exposed group following GD 15–21 irradiation. As a result, a 900-MHz EMF application at GD 15–21, which coincides with hippocampal neurogenesis, triggered hippocampal neuron cell death by activating PARP-1 and Caspase-3.</p>\u0000 </div>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143431703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}