Cerebellar abnormalities following hypoxia alone compared to hypoxic-ischemic forebrain injury in the developing rat brain

NEUROBIOLOGY OF DISEASE

卷:41

Article

Biran, Valerie^1,2,3,4,5  Heine, Vivi M.⁶  Verney, Catherine^3,4,5  Sheldon, R. Ann²  Spadafora, Ruggero²  Vexler, Zinaida S.²  Rowitch, David H.^7,8  Ferriero, Donna M.² 

[1] Hop Robert Debre, AP HP, Serv Pediat & Reanimat Neonatales, F-75019 Paris, France

[2] Univ Calif San Francisco, Dept Neurol & Pediat, San Francisco, CA 94143 USA

[3] INSERM, AVENIR R05230HS, U676, Paris, France

[4] Univ Paris 07, Fac Med Denis Diderot, Paris, France

[5] PremUP, Paris, France

[6] Vrije Univ Amsterdam Med Ctr, Dept Child Neurol, Amsterdam, Netherlands

[7] Dept Pediat, Chevy Chase, MD USA

[8] Howard Hughes Med Inst, Chevy Chase, MD USA

关键词: Cerebellum;    Hypoxia;    Ischemia;    Neuronal death;    Purkinje cells;    Granule cells;    White matter;    Development;   

DOI  :  10.1016/j.nbd.2010.09.001

来源: Elsevier

【 摘 要 】

Two-day-old (P2) rat pups were subjected to either a global hypoxia or to electrocoagulation of the right carotid artery followed by 2.5 h hypoxia. Cellular and regional injury in the cerebellum (CB) was studied at 1, 2 and 19 days using immunohistology. Following hypoxia and hypoxia-ischemia, all neuronal populations of the CB were damaged in a subset of Purkinje cells. The decrease in the number of interneurons, as well as the thickness of molecular and granular layers was significant following hypoxia. Diffuse white matter damage, with loss of preoligodendrocytes was more severe following hypoxia than hypoxia-ischemia. Global hypoxia in the rat at P2 produces extensive damage to many cell types in different areas of the CB. The addition of unilateral forebrain ischemia does not increase the severity of these changes. Our data provide insight into the mechanisms of the changes observed in the CB of premature newborns. (C) 2010 Elsevier Inc. All rights reserved.

【 授权许可】

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