Breier, BFraser, MChristophidis, Larissa2011-06-092011https://hdl.handle.net/2292/6781Very preterm birth disrupts development of the brain and enhances its vulnerability to injury, resulting in neurological impairments ranging in severity from cerebral palsy to mild cognitive deficits. Currently there is no treatment available. Unilateral hypoxic-ischemia (HI) in the three day old rat is well established as a model of brain injury in infants born at 22 to 26 gestational weeks. However, it is inherently variable. I show that this injury results in short term neurological deficits which may be capitalised upon for allocation of pups into treatment studies. After it is injured, the brain tries to repair itself using processes that are a recapitulation of those that occur during brain development. Using a model of injury to the immature brain our laboratory has identified roles for the closely related anterior pituitary hormones growth hormone (GH) and prolactin (PRL) in the brain after injury. Though the role of GH in neuroprotection is well demonstrated, little is known of its capacity for neuro-restoration subsequent to injury. I found that GH receptor immunoreactivity is upregulated in the ipsilateral subventricular zone at five days after injury, corresponding both spatially and temporally with injury-induced neurogenesis. Cells immunopositive for the GH receptor included proliferating and neural precursor cells and post-mitotic neuroblasts. Together with the finding from our laboratory that GH stimulates proliferation of embryonic mouse neural stem cells (NSCs), these results indicate a novel role for GH in injury-induced neurogenesis. Whilst PRL is known to exert effects on neural progenitor and glial cells after injury to the central nervous system, its role in development of extra-hypothalamic brain regions has not been examined. Using a novel real time PCR assay I reveal the ontogeny of the long, fully functional PRL receptor isoform in the rat cerebral cortex and find that it parallels that of neurite initiation and outgrowth markers. Indeed, treatment of neurons derived from adult mouse NSCs with PRL increased the number of primary and secondary neurites. These results implicate a role for PRL in development of the cerebral cortex.Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher.https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htmhttps://creativecommons.org/licenses/by-nc-sa/3.0/nz/ThesisCopyright: The authorhttp://purl.org/eprint/accessRights/OpenAccessQ112885932