Microglia are the resident immunocompetent cells of the central nervous system (CNS). They are extremely plastic and are critical for neurogenesis, circuit structure and function, and play a crucial role in early synapse formation. It is thought that metabotropic glutamate receptor 5 (mGluR5) plays a role in the modulation of microglial phenotype. In this thesis, we assessed the impact of the mGluR5 acting negative allosteric drug, (2-chloro-4-[2[2,5-dimethyl-1-[4-(trifluoromethoxy) phenyl] imidazol-4-yl] ethynyl] pyridine (CTEP), alone and the context of the inflammatory endotoxin, lipopolysaccharide (LPS) upon BV2 cells. This was done to assess if mGluR5 plays a role in microglia phenotype modulation. It was found that LPS has an effect on the expression of mGluR5, but otherwise did not have a significant impact upon other markers. This thesis is a starting point for future studies that seek to determine the role of mGluR5 glutamatergic signaling upon microglial phenotype.