Disturbances in the prenatal environment have been postulated to play a role in the pathogenesis of conditions such as schizophrenia and autism later in life. For example in preeclampsia and intra-uterine growth restriction, where there is a change in oxygen flow to the foetus, resulting in short term hypoxia, have been linked with a higher incidence in schizophrenia and foetal growth restrictions. The excitatory amino acid glutamate is involved in many cellular and physiological processes. In many neurological disorders, glutamate is implicated as being over expressed, and may be the key molecule that could cause dendrite shortening and simplification of the neurones. For this reason during pregnancy, it is important to regulate the levels of glutamate the foetus is exposed to. We used first trimester placental tissue and a primary trophoblast cell barrier model to condition media after the effects of 2%, 21% and 2-8% and 2-21% oxygen changes. This media was then applied to E18.5 rat cortical cultures after 12 days in vitro and found to cause reductions in dendrite lengths, as measured via MAP2 staining and GFP transfections, after 6 days of exposures. In addition, the neurones were also simplified in structure and found to contain fewer spines, therefore impacting on their action potentials and their ability communicate with one another. On analysis of the media, we found a specific and significant increase in glutamate when the tissue was exposed to hypoxia and reoxygenation. We then probed the reason to the mechanism of this release. There are five glutamate transporters within the human body (EAAT1-5), interestingly, 3 of which are only found in the placenta, further highlighting the importance for the regulation of glutamate during pregnancy. We used pharmacological interventions to block these transporters, DL-TBOA, a glutamate transporter antagonist, and DHA, a specific EAAT2 blocker. The results found that DHA being specific to only one transporter was not efficient in blocking the effects on the dendrites. However, DL-TBOA’s actions being non-specific, was found to considerably rescue the dendrite lengths. We hope that our findings and future work could lead to a potential therapy, by inhibiting the effects of glutamate, so that it does not pose a risk to the developing foetus. By understanding the mechanism of release, we aim to pave the way in developing a drug that is able to offer protection to the developing foetus and to reduce the risk of causing the onset of neurological disorders.