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• W3199184411 abstract "Brain injuries such as stroke and birth asphyxia cause major physical and cognitive disabilities.Accumulating evidence shows that the injured brain produces growth factors as an endogenousprotective and regenerative mechanism. Several of these factors have been identified and includeinsulin-like growth factor-I, transforming growth factor and fibroblast growth factor. Recentwork in our laboratory has shown that the growth hormone axis is also upregulated followinghypoxic ischemic injury to the juvenile rat brain. Importantly, central treatment with growthhormone offered strong neuroprotection in this model.In vitro studies reported in this thesis have confirmed the neuroprotective properties of growthhormone. Growth hormone-induced neuroprotection occurs via a neuronal brain-specific growthhormone receptor, which behaves differently from that found in the periphery. Whereas bothligands are strongly somatogenic in the periphery, rat but not bovine growth hormone had strongneuroprotective, neurotrophic and gliatrophic effects in cortical primary cultures. This distinctligand specificity agrees with previous in vivo studies in our laboratory. Further, I show for thefirst time that the prolactin axis, which is closely related to the growth hormone axis, is alsoupregulated within the injured brain. Surprisingly, central treatment with prolactin failed to offerneuroprotection. Immunohistochemistry however showed that prolactin and its receptor werestrongly and primarily upregulated on reactive glia in the penumbra, with limited staining onneurons. This neuronal staining contrasts with a persistent and intense staining for the growthhormone receptor and the growth hormone binding protein on these cells. The lack of anyneuroprotective effect of prolactin in vivo was confirmed using primary cortical cultures. In thesecultures, prolactin had only gliatrophic effects. These findings indicate a primary role forprolactin in glial wound responses following brain injury. Furthermore, the prolactin axis wasupregulated in the neurogenic subventricular zone and dentate gyrus following hypoxia ischemia.In a spatio-temporal fashion, the increased prolactin and prolactin receptor immunoreactivity wasspecifically associated with an increased neuroblast proliferation and migration within theneurogenic regions. A strong association between the prolactin axis and neuroblast activity wasalso seen in neuroblast migration routes. Interestingly, subsequent in vitro studies by T. Gorba inour laboratory confirmed that PRL has strong and direct proliferative and migratory effects onneural stem cells.In summary, these findings show for the first time that the growth hormone and prolactin axesihave distinct roles in the injured brain. The growth hormone axis provides neuroprotectionthrough a distinct neuronal growth hormone receptor. In contrast, the prolactin axis is associatedwith glial wound repair responses, post-injury neurogenesis and neuroblast emigration. Since this…" @default.
• W3199184411 created "2021-09-27" @default.
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• W3199184411 date "2006-01-01" @default.
• W3199184411 modified "2023-09-23" @default.
• W3199184411 title "Protection and recovery of the injured brain the significance of the cerebral growth hormone and prolactin axes" @default.
• W3199184411 hasPublicationYear "2006" @default.
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