Developmental Neuroscience最新文献

{"title":"Hypothermia Treatment after Hypoxia-Ischemia in Glutathione Peroxidase-1 Overexpressing Mice.","authors":"R Ann Sheldon, Christine Windsor, Fuxin Lu, Nicholas R Stewart, Xiangning Jiang, Donna M Ferriero","doi":"10.1159/000531204","DOIUrl":"10.1159/000531204","url":null,"abstract":"<p><p>The developing brain is uniquely susceptible to oxidative stress, and endogenous antioxidant mechanisms are not sufficient to prevent injury from a hypoxic-ischemic challenge. Glutathione peroxidase (GPX1) activity reduces hypoxic-ischemic injury. Therapeutic hypothermia (HT) also reduces hypoxic-ischemic injury, in the rodent and the human brain, but the benefit is limited. Here, we combined GPX1 overexpression with HT in a P9 mouse model of hypoxia-ischemia (HI) to test the effectiveness of both treatments together. Histological analysis showed that wild-type (WT) mice with HT were less injured than WT with normothermia. In the GPX1-tg mice, however, despite a lower median score in the HT-treated mice, there was no significant difference between HT and normothermia. GPX1 protein expression was higher in the cortex of all transgenic groups at 30 min and 24 h, as well as in WT 30 min after HI, with and without HT. GPX1 was higher in the hippocampus of all transgenic groups and WT with HI and normothermia, at 24 h, but not at 30 min. Spectrin 150 was higher in all groups with HI, while spectrin 120 was higher in HI groups only at 24 h. There was reduced ERK1/2 activation in both WT and GPX1-tg HI at 30 min. Thus, with a relatively moderate insult, we see a benefit with cooling in the WT but not the GPX1-tg mouse brain. The fact that we see no benefit with increased GPx1 here in the P9 model (unlike in the P7 model) may indicate that oxidative stress in these older mice is elevated to an extent that increased GPx1 is insufficient for reducing injury. The lack of benefit of overexpressing GPX1 in conjunction with HT after HI indicates that pathways triggered by GPX1 overexpression may interfere with the neuroprotective mechanisms provided by HT.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"98-111"},"PeriodicalIF":2.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10667569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10156194","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":"From Early Motor Ability to Global Cognitive Development 7 Years after Neonatal Arterial Ischemic Stroke.","authors":"Antoine Giraud, Pauline Garel, Brian H Walsh, Stéphane Chabrier","doi":"10.1159/000533816","DOIUrl":"10.1159/000533816","url":null,"abstract":"<p><p>The developmental condition of children after neonatal arterial ischemic stroke (NAIS) is characterized by cognitive and motor impairments. We hypothesized that independent walking age would be a predictor of later global cognitive functioning in this population. Sixty-one children with an available independent walking age and full-scale intelligence quotient (IQ) score 7 years after NAIS were included in this study. Full-scale IQ was assessed using the fourth edition of the Wechsler Intelligence Scale for Children (WISC-IV). Independent walking age was negatively correlated with full-scale IQ score at 7 years of age (Pearson correlation coefficient of -0.27; 95% confidence interval from -0.48 to -0.01; p &lt; 0.05). Early motor function is correlated with later global cognitive functioning in children after NAIS. Assessing and promoting early motor ability is essential in this population.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"149-152"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11151956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10476395","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":"Prelims","authors":"Dr. Amy Malik","doi":"10.1159/000535086","DOIUrl":"https://doi.org/10.1159/000535086","url":null,"abstract":"","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"81 4","pages":"309 - 312"},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138986363","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":"Front & Back Matter","authors":"","doi":"10.1159/000531303","DOIUrl":"https://doi.org/10.1159/000531303","url":null,"abstract":"","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45406985","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":"Front & Back Matter","authors":"","doi":"10.1159/000531306","DOIUrl":"https://doi.org/10.1159/000531306","url":null,"abstract":"","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45644260","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":"Beyond the Rainbow: A Review of Advanced Lineage Tracing Methodologies for Interrogating the Initiation, Evolution, and Recurrence of Brain Tumors","authors":"Sara Sabet, Joshua J. Breunig","doi":"10.1159/000530329","DOIUrl":"https://doi.org/10.1159/000530329","url":null,"abstract":"The mammalian forebrain is perhaps the pinnacle of evolution and one of the most complex structures in known existence. The origin of this complexity and diversity partly lies in dynamic behavior of progenitors during embryonic neural development, all of which is under the control of regulatory mechanisms that ensure all the elements end up in the right place at the right time. Historically, dye-base, histochemical, enzymatic, or fluorescent lineage tracing techniques have been used deconvolute developmental dynamics in tissues and cells. Technical limitations resulted from a restrictive number of fluorophores, the half-life of the dyes, or the ability to deconvolute mixed population. These limitations often impede larger scale lineage tracing using these methods in spatial and temporal contexts. Genetic barcoding techniques have been used for decades to explore clonal investigations and have now evolved with high-throughput sequencing methods to allow for impressive insights into population and even organism-level lineage relationships. In this review, we will discuss the progression of lineage tracing methodologies and how they are applied to answer questions around molecular and cellular mechanisms of gliogenesis and neurogenesis. We will also discuss recent advances in computational biology, single-cell sequencing, and in situ-based lineage tracing methodologies. Incorporation of these methods into toolset of lineage tracing promise to enable a higher resolution, multimodal view of neural lineages during development and disease processes that highjack developmental signaling such as brain tumor development and recurrence – where traditional developmental hierarchies become more plastic and less predictable. Given the dismal prognosis of high-grade brain tumors like glioblastoma multiforme, a better understanding of the lineage relationships leading to disease heterogeneity and recurrence is desperately needed to formulate efficacious approaches to treatment. Here we discuss a historical foundation on, as well as the future of, lineage tracing at the intersection of development and disease.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"45 1","pages":"181 - 190"},"PeriodicalIF":2.9,"publicationDate":"2023-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49022988","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":"Acknowledgement to Reviewers","authors":"","doi":"10.1159/000529329","DOIUrl":"https://doi.org/10.1159/000529329","url":null,"abstract":"<br />Dev Neurosci 2022;44:678","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"42 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138516251","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":"Front & Back Matter","authors":"A. Campagnoni","doi":"10.1159/000529657","DOIUrl":"https://doi.org/10.1159/000529657","url":null,"abstract":"","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"44 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41737879","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":"Maternal Immune Activation by Polyinosinic-Polycytidylic Acid Exposure Causes Cerebral Cortical Dysgenesis through Dysregulated Cell Cycle Kinetics of Neural Stem/Progenitor Cells","authors":"Marie Sasaki, T. Mitsuhashi, Fumiko Goto, S. Shibata, K. Kubo, Shinju Oku, Akihiro Owashi, Takao Takahashi","doi":"10.1159/000529317","DOIUrl":"https://doi.org/10.1159/000529317","url":null,"abstract":"Maternal immune activation reportedly causes dysregulation of the cell cycle in stem cells and impairment of higher cortical function in rodents. Furthermore, in humans, maternal immune activation during the first to second trimester of pregnancy is strongly correlated with increased incidence of autism spectrum disorder in the offspring. Here, we show that in utero exposure to polyinosinic-polycytidylic acid (poly (I:C)) in mice during the early phase of neuronogenesis increases the probability of differentiation (quiescent fraction [Q fraction]) of neural stem/progenitor cells (NSPCs) without change in the length of cell cycle. This abnormal increase in the Q fraction is assumed to reduce the peak population size of NSPCs, resulting in the thinning of the neocortex in offspring because of the reduced production of neurons. Furthermore, the neocortex of poly (I:C)-exposed mice does not exhibit a layer-specific reduction in radial thickness, possibly because of increased apoptosis caused by poly (I:C) exposure during all stages of cortical development. These results suggest that maternal immune activation by poly (I:C) exposure may affect neocortical histogenesis by altering the cell cycle kinetics of NSPCs. In addition, the timing and amount of poly (I:C) exposure during pregnancy may have profound effects on cerebral cortical histogenesis.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"45 1","pages":"115 - 125"},"PeriodicalIF":2.9,"publicationDate":"2023-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47507709","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":"Auditory Outcomes in Adolescents with Prenatal Alcohol Exposure.","authors":"Humberto de Oliveira Simões,&nbsp;Eduardo Tanaka Massuda,&nbsp;Erikson Felipe Furtado,&nbsp;Sthella Zanchetta","doi":"10.1159/000528846","DOIUrl":"https://doi.org/10.1159/000528846","url":null,"abstract":"<p><p>The aim of the study was to investigate three aspects of auditory function (auditory acuity, cochlear dysfunction, and auditory processing) in adolescents with fetal alcohol exposure without phenotypic changes. Fifty-one adolescents with and without intrauterine exposure to alcohol were selected from a cohort study. The summons, evaluation, and analysis of the results were carried out blindly regarding the respective exposure to alcohol. The auditory tests were pure-tone audiometry, transient otoacoustic emissions, and behavioral assessment of auditory processing (speech-in-noise, dichotic digits, and gap-in-noise). After testing, 45 adolescents were included in the evaluation and were divided into exposed (n = 22) and non-exposed (n = 23) groups. Hearing loss was identified in one subject in the exposed group (4.5%). In the absence of hearing loss, there were no significant differences in tonal thresholds or in the magnitudes of the sensory (cochlear) responses between groups (p > 0.05). There was also no difference between the two groups regarding performance on the processing tests (speech-in-noise p = 0.71, dichotic p = 0.94, and gap-in-noise p = 0.33). However, the exposed group had more cases of hearing disorders (hearing loss plus auditory processing disorders) than the non-exposed group (22.7% vs. 4.3%).</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"45 1","pages":"27-36"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10129020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9678251","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}