Presentation description

Epilepsy is a devastating neurological disorder affecting nearly three million people in the U.S.
and is characterized by recurrent unprovoked seizures, which can result from numerous brain
injuries. Encephalitis is a neuroinflammatory condition and a major risk factor for seizures and
epilepsy, with over 100 different viruses known to have caused encephalitis in humans. When
injected into the cortex of the C57/Bl6 mice, Theiler's Murine Encephalomyelitis Virus (TMEV)
causes acute seizures 3-8 days post infection (dpi), pyramidal neuron death, and reactive gliosis
in the CA1 region of the hippocampus; these mice can then go on to develop chronic epilepsy.
Thus, the TMEV infection model of temporal lobe epilepsy (TLE) is an etiologically relevant
mouse model. Among the neuroimmune glial cells of the brain, reactive astrocytes have been
shown to phagocytose and break down neuronal material. Our study aims to determine if
astrocytic phagolysosomal activity increases during acute TMEV infection. We used
immunohistochemical methods to stain brain sections from TMEV and PBS treated mice with
antibodies against glial fibrillary acidic protein (GFAP) for astrocytes and lysosome-associated
membrane glycoprotein 2 (Lamp2) for phagolysosomes. We then reconstructed astrocytes in the
CA1 region of the hippocampus using Imaris software and quantified the amount of Lamp2
signal within the cell volumes. On-going analysis will compare the average amount of astrocytic
Lamp2 signal, as a function of Intensity Sum per Volume, between TMEV and PBS conditions.
We will determine if astrocytic phagolysosomal activity increases in TMEV treatment, thus
contributing to hippocampal maintenance following infection.