Schizophrenia is a severally debilitating conditions affecting approximately 1% of the world’s population. While there is no defining sign or symptom of schizophrenia the range of symptoms can be classified as positive (e.g. hallucinations), cognitive (e.g. impaired memory) and negative (e.g. social incompetence). Despite having 0.8 heritability Schizophrenia has no classical Mendelian inheritance patterns or fully penetrant genes. The highly homogenous nature of Schizophrenia has lead to a variety of theories as to its etiology with the current prevailing evidence suggesting a developmental insult leading to hyper levels of glutamate and hypo-function of the NMDA receptors of the glutamatergic system(1). It has recently been found by our group that the placental tissue when exposed to hypoxic conditions releases an increased concentration of glutamate(2) into the surrounding media. It was hypothesised that this glutamate release might alter the presentation and function of receptors in the developing brain. To investigate this, human first trimester placental explants were exposed to oxygen concentrations of 2-8% and 21% in neurobasal media which was then collected. Cortical neurones from e18 rats were cultured on Poly-L-Lysine coated coverslips for 12 days then exposed to the conditional media for 7 days before fixation. Other neuronal cultures were similarly grown then exposed to varying concentrations of glutamate. Fluorescent immunostaining was performed on permalised and non-permalised cultures using antibodies for NMDA R1, NR3A, GABA A α1 and GABA B1. These targets were chosen to provide information on the functional capacity of the excitatory and inhibitory systems in the cultures. It was found that increasing the concentration of glutamate leads to a reduction in the detection of NMDA R1 and an increase in the detection of NR3A. This would indicate that the increase in glutamate is causing the neurones to reduce the number and function of NMDA receptors(3). This effect was mirrored when using hypoxia conditioned media where 2-8% conditioned media resulted in increased detection of NR3A and reduced levels of NMDA R1. These finding correspond to those found in post mortem studies of patients with schizophrenia(4). The increased levels of hypoxia and glutamate were shown to cause a reduction in the presentation of GABA A α1 and an increase in the presentation of GABA B1 suggesting a deregulation of the gabaergenic system(5). This findings suggest that factors, notably glutamate, secreted by the placenta during an hypoxic event cause alterations to the excitatory and inhibitory signalling systems on neurones in a similar manner to that recorded in Schizophrenic patients.