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      Subplate in a rat model of preterm hypoxia–ischemia

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          Abstract

          Objective

          Hypoxia–ischemia (HI) in preterm infants primarily leads to injuries in the cerebral white matter. However, there is growing evidence that perinatal injury in preterms can also involve other zones including the cortical gray matter. In a neonatal rat model of HI, selective vulnerability of subplate has been suggested using BrdU birth-dating methods. In this study, we aimed to investigate the neuropathological changes of the subplate and deep layers of the cortex following cerebral HI in neonatal rats with specific cell markers.

          Methods

          P2 rats underwent permanent occlusion of the right common carotid artery followed by a period of hypoxia. P8 rats were analyzed using immunohistochemistry; subplate and deep layers cells were quantified and compared with sham-operated case.

          Results

          A large variability in the extent of the cerebral injury was apparent. For the three analyzed subplate populations (Nurr1+, Cplx3+, and Ctgf+ cells), no significant cell reduction was observed in mild and moderate cases. Only in severe cases, subplate cells were strongly affected, but these injuries were always accompanied by the cell reductions in layers VI and V.

          Interpretation

          We could therefore not confirm a specific vulnerability of subplate cells compared to other deep layers or the white matter in our model.

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          Pathogenesis of cerebral white matter injury of prematurity.

          O Khwaja, J J Volpe (2008)
          Cerebral white matter injury, characterised by loss of premyelinating oligodendrocytes (pre-OLs), is the most common form of injury to the preterm brain and is associated with a high risk of neurodevelopmental impairment. The unique cerebrovascular anatomy and physiology of the premature baby underlies the exquisite sensitivity of white matter to the abnormal milieu of preterm extrauterine life, in particular ischaemia and inflammation. These two upstream mechanisms can coexist and amplify their effects, leading to activation of two principal downstream mechanisms: excitotoxicity and free radical attack. Upstream mechanisms trigger generation of reactive oxygen and nitrogen species. The pre-OL is intrinsically vulnerable to free radical attack due to immaturity of antioxidant enzyme systems and iron accumulation. Ischaemia and inflammation trigger glutamate receptor-mediated injury leading to maturation-dependent cell death and loss of cellular processes. This review looks at recent evidence for pathogenetic mechanisms in white matter injury with emphasis on targets for prevention and treatment of injury.
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            Selective vulnerability of late oligodendrocyte progenitors to hypoxia-ischemia.

            N. Luo, B. H. Han, David Holtzman … (2002)
            In the premature infant, hypoxic-ischemic damage to the cerebral white matter [periventricular leukomalacia (PVL)] is a common and leading cause of brain injury that often results in chronic neurologic disability from cerebral palsy. The cellular basis for the propensity of white matter injury to occur in the developing brain and the greater resistance of the adult white matter to similar injury remains unknown. By using a neonatal rat model of hypoxic-ischemic injury, we found that the mechanism of perinatal white matter injury involved maturation-dependent vulnerability in the oligodendroctye (OL) lineage. The timing of appearance of late OL progenitors was the major developmental factor that accounted for the susceptibility of the neonatal white matter to injury. Late OL progenitors were the major OL lineage stage killed by apoptosis, whereas early OL progenitors and more mature OLs were highly resistant. The density of pyknotic late OL progenitors was significantly increased in the ischemic hemisphere (67 +/- 31 cells/mm2) versus the control hemisphere (2.2 +/- 0.4 cells/mm2; mean +/- SEM; p = 0.05), which resulted in the death of 72 +/- 6% of this OL stage. Surviving late OL progenitors displayed a reactive response in which an increase in cell density was accompanied by accelerated maturation to a P27/kip1-positive oligodendrocyte. Because we showed recently that late OL progenitors populate human cerebral white matter during the high risk period for PVL (Back et al., 2001), maturation-dependent vulnerability of OL progenitors to hypoxia-ischemia may underlie the selective vulnerability to PVL of the white matter in the premature infant.
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              Laminar organization of the human fetal cerebrum revealed by histochemical markers and magnetic resonance imaging.

              Ivica Kostović, Miloš Judaš, Marko Radoš … (2002)
              The developing human cerebrum displays age-specific changes in its patterns of lamination. Among these, the subplate zone is the most prominent transient compartment because growing major afferent systems temporarily reside in this zone, establish synapses and take part in cellular interactions that are crucial for subsequent cortical development. We explored the potential of magnetic resonance imaging (MRI) for tracing the developmental history of the most prominent cortical layer (the subplate zone) and other laminar compartments of the fetal cerebral wall between 15 and 36 weeks post-ovulation. We found that changes in the MRI lamination pattern of the human fetal cerebral wall are predominantly caused by changes in the subplate zone. Histochemical staining of the extracellular matrix (ECM) enables selective visualization of the subplate zone and correlation with an increase in MRI signal intensity in the subplate zone and ingrowth and accumulation of thalamocortical and corticocortical afferents and their subsequent relocation to the cortical plate. Thus, dynamic changes in the MRI appearance of the subplate zone and histochemical staining of its ECM can be used as indirect parameters for an assessment of normal versus disturbed unfolding of crucial histogenetic events that are involved in prenatal shaping of the human cerebral cortex.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Clin Transl Neurol
                Journal ID (iso-abbrev): Ann Clin Transl Neurol
                Journal ID (publisher-id): acn3
                Title: Annals of Clinical and Translational Neurology
                Publisher: BlackWell Publishing Ltd (Oxford, UK )
                ISSN (Print): 2328-9503
                ISSN (Electronic): 2328-9503
                Publication date (Print): September 2014
                Publication date (Electronic): 30 September 2014
                Volume: 1
                Issue: 9
                Pages: 679-691
                Affiliations
                [1 ]Department of Physiology, Anatomy and Genetics, University of Oxford Oxford, United Kingdom
                [2 ]Institute for Advanced Medical Sciences, Hyogo College of Medicine Hyogo, Japan
                [3 ]Division of Neonatology, Department of Pediatrics, University Hospital Center and University of Lausanne Lausanne, Switzerland
                Author notes
                Correspondence: Zoltán Molnár, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom. Tel: +44 1865 282664; Fax: +44 1865 272488; E-mail: zoltan.molnar@ 123456dpag.ox.ac.uk

                Funding Information: This work is supported by the MRC (UK), the Berrow Foundation (Lincoln College, Oxford University), and the Eagle Foundation (Switzerland). We are grateful to Ann Sheldon and Donna Ferriero (University of California San Francisco, Neurointensive Care Nursery, 505 Parnassus Ave., 15th floor, San Francisco, CA 94143, USA) for providing material for Figure S2 and for discussions.

                [a]

                Contributed equally.

                Article
                DOI: 10.1002/acn3.97
                PMC ID: 4241795
                PubMed ID: 25493282
                SO-VID: 36f6a01a-0d0a-4d6e-8df1-d4460e734005
                Copyright © © 2014 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.
                License:

                This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 07 May 2014
                Date accepted : 25 July 2014
                Categories
                Subject: Research Articles

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