Neonatal hypoxic-ischemic encephalopathy (HIE) is a serious condition in which the developing brain does not receive enough oxygen and blood flow during the perinatal period. It is a leading cause of infant mortality and the development of later-life sequelae, including cerebral palsy, learning disabilities, and paediatric epilepsy. Microglia, the resident immune cells in the central nervous system, are key drivers of neuroinflammation in response to injury. However, they also play an essential role in shaping neural networks during development, suggesting that microglial dysfunction may link acute injury to long-term neurological deficits. Here, publicly available single-cell RNA-seq data from a mouse model of maternal immune activation and hypoxia were analysed to evaluate changes in microglial gene expression. Analysis was performed in R using the Seurat package. A range of genes were found to be differentially expressed between normoxic and hypoxic microglia. Notably, Slc1a3, the gene encoding the glutamate transporter known as GLAST, was lower in hypoxic microglia (p = 1.54×10^-35). Moreover, the GABA_B receptor subunit encoded by Gabbr1 was also decreased in hypoxic microglia (p = 0.002). Pathway enrichment analysis of upregulated genes in the normoxic cells revealed several neurotransmission-related processes, including neurotransmitter receptors and postsynaptic signal transmission (p = 2.06×10^-5). These findings suggest that genes involved in neuronal signalling, such as glutamate transporters and GABA receptor subunits, are relatively reduced following hypoxia. Overall, hypoxia may shift microglial gene expression away from homeostatic, synapse-related functions. Ultimately, a better understanding of the microglial response to HIE could inform new therapies.