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Increased cell proliferation in the rat anterior cingulate cortex following neonatal hypoxia: relevance to schizophrenia

Please always quote using this URN: urn:nbn:de:bvb:20-opus-125890
  • As a consequence of obstetric complications, neonatal hypoxia has been discussed as an environmental factor in the pathophysiology of schizophrenia. However, the biological consequences of hypoxia are unclear. The neurodevelopmental hypothesis of schizophrenia suggests that the onset of abnormal brain development and neuropathology occurs perinatally, whereas symptoms of the disease appear in early adulthood. In our animal model of chronic neonatal hypoxia, we have detected behavioral alterations resembling those known from schizophrenia.As a consequence of obstetric complications, neonatal hypoxia has been discussed as an environmental factor in the pathophysiology of schizophrenia. However, the biological consequences of hypoxia are unclear. The neurodevelopmental hypothesis of schizophrenia suggests that the onset of abnormal brain development and neuropathology occurs perinatally, whereas symptoms of the disease appear in early adulthood. In our animal model of chronic neonatal hypoxia, we have detected behavioral alterations resembling those known from schizophrenia. Disturbances in cell proliferation possibly contribute to the pathophysiology of this disease. In the present study, we used postnatal rats to investigate cell proliferation in several brain areas following neonatal hypoxia. Rats were repeatedly exposed to hypoxia (89 % N2, 11 % O2) from postnatal day (PD) 4–8. We then evaluated cell proliferation on PD 13 and 39, respectively. These investigations were performed in the anterior cingulate cortex (ACC), caudate-putamen (CPU), dentate gyrus, and subventricular zone. Rats exposed to hypoxia exhibited increased cell proliferation in the ACC at PD 13, normalizing at PD 39. In other brain regions, no alterations have been detected. Additionally, hypoxia-treated rats showed decreased CPU volume at PD 13. The results of the present study on the one hand support the assumption of chronic hypoxia influencing transient cell proliferation in the ACC, and on the other hand reveal normalization during ageing.show moreshow less

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Metadaten
Author: Evelin L. Schaeffer, Franziska Kühn, Angelika Schmitt, Wagner F. Gattaz, Oliver Gruber, Thomas Schneider-Axmann, Peter Falkai, Andrea Schmitt
URN:urn:nbn:de:bvb:20-opus-125890
Document Type:Journal article
Faculties:Medizinische Fakultät / Klinik und Poliklinik für Psychiatrie, Psychosomatik und Psychotherapie
Language:English
Parent Title (English):Journal of Neural Transmission
Year of Completion:2013
Volume:120
Issue:1
Pagenumber:187-195
Source:Journal of Neural Transmission (2013) 120:187–195 DOI 10.1007/s00702-012-0859-y
DOI:https://doi.org/10.1007/s00702-012-0859-y
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:anterior cingulate cortex; cell proliferation; neonatal hypoxia; rat; schizophrenia
Release Date:2016/07/12
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung