Inherent to the pathophysiology of both ischemic and haemorrhagic stroke is the depletion of tissue oxygen levels. While brain ischaemia can elicit irreparable brain injury, it primes a defence mechanism to boost the formation of new neurons from known neural precursor cell niches in the adult brain, contributing to repair and partial recovery of brain function. Fuller understanding of this mechanism could inform therapeutic strategies to enhance this endogenous repair process. Hypoxic microenvironments stabilise hypoxia-inducible factor 1-alpha (HIF1-α), reported to independently promote key stem/precursor-cell protection and regulatory pathways involving Nrf2 and Notch1 signalling. In the present study, these signalling events have been investigated as a possible mechanism underlying hypoxia-induced neurogenesis. Human neuroblastoma cells (SH-SY5Y), possessing neural precursor properties, were exposed to room air (18kPa O2) or hypoxia (1kPa O2) for 2 – 72h. Whole-cell lysates were immunoblotted for HIF-1α, Notch1 full-length and intracellular domain as well as Nrf2 and its downstream targets heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase quinone 1 (NQO1). We also assessed cell viability, proliferation and redox signalling in cells loaded with L-012 followed by exposure to hypoxia (1h) and reoxygenation (1h). Cell viability was unaffected by hypoxia but proliferation decreased after 72h hypoxia (18 kPa 37.97±3.43x106cells/ml vs 1 kPa 1.13±3.23x106cells/ml, n= 4, P<0.05). After 2h, HIF1-α protein levels were increased significantly and remained elevated until 16h. Full-length Notch1 protein expression was also elevated by hypoxia, while Nrf2 and downstream targets HO1 and NQO1 were unaffected. Acute hypoxia alone did not stimulate L-O12 luminescence but subsequent reoxygenation increased L-012 luminescence, which was abrogated by PEG-SOD and unaffected by PEG-CAT, both reactive oxygen species (ROS) scavengers. Our findings confirm HIF1-α stabilisation following hypoxia and changes to Notch1 expression in human neuroblast-like cells. Conversely, neither hypoxia-induced neuroblast proliferation nor Nrf2-signalling changes were found, contrary to previous reports. Ongoing experiments are investigating changes in neurogenic-markers and notch1-downstream signalling. Supported by MRC-DTP PhD Studentship