16
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Histology Atlas of the Developing Prenatal and Postnatal Mouse Central Nervous System, with Emphasis on Prenatal Days E7.5 to E18.5

      1 , 2 , 3 , 2 , 4 , 5 , 6 , 4
      Toxicologic Pathology
      SAGE Publications

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          <p class="first" id="P1">Evaluation of the central nervous system (CNS) in the developing mouse presents unique challenges given the complexity of ontogenesis, marked structural reorganization over very short distances in three dimensions each hour, and numerous developmental events susceptible to genetic and environmental influences. Developmental defects affecting the brain and spinal cord arise frequently both <i>in utero</i> and perinatally as spontaneous events, following teratogen exposure, and as sequelae to induced mutations, and thus are a common factor in embryonic and perinatal lethality in many mouse models. Knowledge of normal organ and cellular architecture and differentiation throughout the mouse’s lifespan is crucial to identify and characterize neurodevelopmental lesions. By providing a well-illustrated overview summarizing major events of normal <i>in utero</i> and perinatal mouse CNS development with examples of common developmental abnormalities, this annotated, color atlas can be used to identify normal structure and histology when phenotyping genetically engineered mice (GEM) and will enhance efforts to describe and interpret brain and spinal cord malformations as causes of mouse embryonic and perinatal lethal phenotypes. The schematics and images in this atlas illustrate major developmental events during gestation from embryonic day (E) 7.5 to E18.5 and after birth from postnatal day (P)1 to P21. </p>

          Related collections

          Most cited references157

          • Record: found
          • Abstract: found
          • Article: not found

          Fate mapping analysis reveals that adult microglia derive from primitive macrophages.

          Microglia are the resident macrophages of the central nervous system and are associated with the pathogenesis of many neurodegenerative and brain inflammatory diseases; however, the origin of adult microglia remains controversial. We show that postnatal hematopoietic progenitors do not significantly contribute to microglia homeostasis in the adult brain. In contrast to many macrophage populations, we show that microglia develop in mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice. In vivo lineage tracing studies established that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8. These results identify microglia as an ontogenically distinct population in the mononuclear phagocyte system and have implications for the use of embryonically derived microglial progenitors for the treatment of various brain disorders.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            The cell biology of neurogenesis.

            During the development of the mammalian central nervous system, neural stem cells and their derivative progenitor cells generate neurons by asymmetric and symmetric divisions. The proliferation versus differentiation of these cells and the type of division are closely linked to their epithelial characteristics, notably, their apical-basal polarity and cell-cycle length. Here, we discuss how these features change during development from neuroepithelial to radial glial cells, and how this transition affects cell fate and neurogenesis.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across species.

              Hypoxic-ischemic and traumatic brain injuries are leading causes of long-term mortality and disability in infants and children. Although several preclinical models using rodents of different ages have been developed, species differences in the timing of key brain maturation events can render comparisons of vulnerability and regenerative capacities difficult to interpret. Traditional models of developmental brain injury have utilized rodents at postnatal day 7-10 as being roughly equivalent to a term human infant, based historically on the measurement of post-mortem brain weights during the 1970s. Here we will examine fundamental brain development processes that occur in both rodents and humans, to delineate a comparable time course of postnatal brain development across species. We consider the timing of neurogenesis, synaptogenesis, gliogenesis, oligodendrocyte maturation and age-dependent behaviors that coincide with developmentally regulated molecular and biochemical changes. In general, while the time scale is considerably different, the sequence of key events in brain maturation is largely consistent between humans and rodents. Further, there are distinct parallels in regional vulnerability as well as functional consequences in response to brain injuries. With a focus on developmental hypoxic-ischemic encephalopathy and traumatic brain injury, this review offers guidelines for researchers when considering the most appropriate rodent age for the developmental stage or process of interest to approximate human brain development. Copyright © 2013 Elsevier Ltd. All rights reserved.
                Bookmark

                Author and article information

                Journal
                Toxicologic Pathology
                Toxicol Pathol
                SAGE Publications
                0192-6233
                1533-1601
                September 11 2017
                August 2017
                September 11 2017
                August 2017
                : 45
                : 6
                : 705-744
                Affiliations
                [1 ]Charles River Laboratories Inc., Durham, North Carolina, USA
                [2 ]Authors contributed equally
                [3 ]Charles River Laboratories Inc., Shrewsbury, Massachusetts, USA
                [4 ]Cellular Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
                [5 ]Bio-Molecular Screening Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
                [6 ]GEMpath Inc., Longmont, Colorado, USA
                Article
                10.1177/0192623317728134
                5754028
                28891434
                8343cd77-b2e2-4319-a3ab-d84c37154ca2
                © 2017

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

                History

                Comments

                Comment on this article