The aim of this project was to characterise a first-generation polymer enzyme composite (PEC) biosensor for monitoring brain extracellular glucose. The brain is heavily dependent on glucose as its primary energy source and dysregulation of metabolism is linked to several neurological disorders including neurogenerative diseases such as Alzheimer’s. Therefore, quantification and an improved understanding of glucose changes and their relationship to other metabolites in the brain, are important research goals. This project involved applying the composite biosensor design that has previously been used to monitor other neurochemicals such as D-serine, choline, glutamate and lactate to the existing glucose biosensor design that was previously developed by Lowry et al. The core components of different crosslinking/stabilising agents, layering strategies and drying times for the PEC biosensor design have already been optimised in the previously developed devices. When the composite design was applied for the detection of glucose the chosen sensor design was: PtD(PoPD)(Sty)(GOx/GA)15 Where a PtD electrode (Platinum disc) was modified with PoPD (poly-ophenylenediamine), an interference rejection layer, Sty (Styrene) an immobiliser, GOx (glucose oxidase) the enzyme and finally GA (glutaraldehyde) a cross-linking agent. Firstly, a literature review of neurochemical glucose biosensors was conducted to compare and contrast the new glucose biosensor’s response characteristics (e.g. sensitivity, Vmax and Km) with devices already reported. An in vitro characterisation of the composite glucose biosensor was performed to determine the sensitivity of the device. The sensor was exposed to a range of pH and temperatures that it may encounter in the brain. Oxygen dependence studies were performed to ensure the low O2 concentration in the brain would not hinder the biosensor’s performance. Biocompatibility tests were conducted as exposure to brain tissue can lead to a decrease in sensitivity due to electrode poisons, surfactants and surface modifying agents. A range of different stability experiments were performed to determine the effect repeat calibrations had on the sensitivity of the biosensor along with shelf-life experiments to assess the longevity of the device. Finally, interference rejection was tested for common endogenous electroactive interferents to ensure they had minimal effect on the glucose signal recorded. In summary, the polymer enzyme composite biosensor achieved an excellent sensitivity of 32.42 ± 0.90 nA.cm-2.μM-1. It had a shelf-life of several weeks and no loss of sensitivity was observed after repeat calibrations or exposure to ex vivo rodent brain tissue (14 days). The sensor performed adequately under all physiologically relevant pH and temperature ranges. The addition of a poly-ortho-phenylenediamine (PoPD) layer provided the sensor with interference rejection properties which resulted in a reliable, interference-free detection of glucose. Preliminary in vivo studies were performed in freely moving rats where the sensor demonstrated reliable signals in response to neuronal activation (tail pinch), and expected signals were observed when interference testing for ascorbic acid and oxygen was performed. Future work will involve extending the vivo characterisation of the biosensor.