Hypoxic insults during pregnancy can cause damage to the developing foetus. The mechanism is not fully understood but glutamate is thought to play an important role. Hypoxia and hypoxia/reoxygenation during pregnancy are also linked to development of psychological disorders later in life[1]. The placenta is a key interface between mother and foetus. Our previous research has suggested that it may secrete factors including glutamate in vitro after hypoxia and hypoxic/reoxygenation. Secretions caused decreased dendritic length of dissociated embryonic cortical rat neurons in vitro, with altered staining of glutamate and GABA receptors. This project aim is to investigate if placental secretions also affect glial cells, which play a homeostatic role for glutamate. Dissociated cells from cerebral cortex of p18 rats were plated at 10,000 cells/ml on coverslips and cultured for 12 days. Conditioned media was prepared using a model placental barrier of BeWo cells grown on transwell inserts[2]. These were exposed to a 24 hour hypoxic insult (2%), hypoxic reoxygenation (2-8%, 2-21%) event or control (21%). Cortical cells were exposed to the conditioned media, Glutamate (100uM, 500uM) or a neurobasal media control for 7 days. The cells were stained with Glial Fibrillary Acidic Protein (GFAP) and cell counts and process lengths were measured with ImageJ. Hypoxic conditioned media caused a 2 fold increase of mean GFAP stained cells from 8±3 GFAP+ cells per field of view (FOV)(x40obj)(neurobasal control) to 16±4 GFAP+ cells (2%). Hypoxic/reoxygenation conditions caused a lesser increase of 10±3 GFAP+ cells/FOV (2-8%). This result was independent of plating density at 10,000 and 50,000 cells/ml. Direct exposure to glutamate alone caused no change in GFAP+ cell count, and a non-significant decrease of astroprocess lengths. Inhibitors of Smad (Noggin), P38 MAPK(SB 203580) and EGF R (PD 168393) were applied in addition to conditioned media to identify the mechanism for this response. This data suggests that response to secretions from the model placental barriers is cell specific. The neurones show a reduction of process length with no change in cell number after exposure to conditioned media from hypoxic or hypoxic reoxygenated BeWo barriers or directly applied glutamate. In contrast astrocytes respond only to conditioned media from hypoxic BeWo barriers and with an increase cell number. These data point to the existence of a second and glial specific factor that may be secreted from the placenta under hypoxic conditions, with potential impact on cell development.