Epilepsy affects 70 million people worldwide and is defined diagnostically as 2 unprovoked seizures within 24 hours. Brain infections can provoke seizures and increase the risk of developing chronic epilepsy through inflammatory pathways. Glial cells are critically involved in neuroinflammation. NG2 glial cells are highly proliferative and involved in myelination, whereas astrocytes maintain the blood-brain barrier and modulate neuron metabolism. We will investigate the impact of deletion of NG2 cells on infection-induced seizures. The effect of NG2 glia deletion on other glia cells is currently unknown and important to determine if absent NG2 cells results in astrocytes becoming reactive before infection. We hypothesize that deletion of NG2 cells will cause astrocytes to become reactive. I used a tamoxifen inducible Cre-ERT2 system to express the diphtheria receptor on NG2 cells for acute cell deletion. Diphtheria was administered intraperitoneally to bind to the receptors and delete NG2 cells. Following diphtheria-induced depletion, animals were sacrificed, and brain sections were acquired for immunohistochemistry and analysis.
Using immunohistochemistry, NG2 cell presence and astrocyte expression after 12 hours and 7 days following administration of diphtheria toxin. Astrocyte reactivity was calculated by comparing the percent area in brain sections obtained from diphtheria treated to control with no expressed receptor. These experiments will inform our basic understanding of the impact of deleting a population of glial cells on neuroinflammation and ultimately on how brain infections can induce epilepsy. Future directions for this research will lead to more understanding of the role of NG2 glia in mechanisms underlying epilepsy.