Almost 50% of individuals diagnosed with immune-mediated inflammatory diseases (IMIDs) such as psoriatic disease exhibit comorbid anhedonic depression. Recent work has found that chronic immune activation plays a causal role in depression by directly impacting neural circuitry underlying motivation. Existing animal models of inflammation generally mimicking acute infection via application of agents such as lipopolysaccharide. They fail to recapitulate the low-grade, chronic inflammation experienced by individuals living with IMIDs. The aim of our work is to develop a chronic model of neuroinflammation by genetically overexpressing TNF-alpha in astrocytes. Our overall goal is to investigate the effects of chronic neuroinflammation on the neural circuitry underlying reward and motivation neural circuitry, and consequent effects on behaviour. We generated a new transgenic mouse model that allows expression of TNF-alpha to be driven in a Cre-dependent manner, and crossed with mice expressing Cre recombinase specifically in astrocytes. We employed tamoxifen-inducible mouse lines to allow control over the fraction of astrocytes that overexpress TNF-alpha. To validate the model, we quantified the level of cytokine expression by glial cells via flow cytometry, and used immunohistochemistry to characterise morphological changes caused by glial reactivity. Pilot experiments using the Aldh1l1-CreERT mouse with varying low doses of tamoxifen revealed widespread neuroinflammation occurring in a dose-dependent manner . Additionally, these mice displayed anxiety-like and reduced exploratory behaviours. However, as Aldh1l1 is also expressed in hepatocytes, a strong TNF-alpha-mediated peripheral response also occurred, confounding the results. We will present pilot data from Aldh1l1-CreERT::TNFa mice as well new data using Glast-CreERT::TNFa mice.