Gregory W. Konat
Centers for Neuroscience
West Virginia University Health Science Center
United States of America
My research interests are primarily focused on innate immunity of the brain. In particular, the research objective of my laboratory is to elucidate mechanisms by which inflammatory episodes in the periphery elicit inflammatory response in the brain and alter its function.
The immune system and the brain maintain intricate communication that plays an important role in both health and disease. For example, epidemiological evidence indicates that peripheral inflammatory conditions are comorbid factors in epilepsy. The putative mechanisms entail pathways by which inflammatory signals are relayed to the brain and lower seizure threshold. However, these pathways have not been defined. We have developed a mouse model to study the effect of viral infections on seizure propensity. In this model, peripheral inflammation is induced by peritoneal injection of dsRNA, a viral mimic. This inflammatory challenge renders the brain hypersusceptible to kainic acid-induced seizures as seen from increased severity and prolonged duration of status epilepticus. Our experimental paradigm provides a valuable heuristic model for unveiling mechanisms by which peripheral inflammatory signals are conveyed to the brain and affect its function.
Hunsberger, H.C., Wang, D., Petrisko, T.J., Alhowail, A., Setti, S.E., Suppiramaniam, V., Konat, G. and Reed, M.N. (2016) Peripherally restricted viral challenge elevates extracellular glutamate and enhances synaptic transmission in the hippocampus. J. Neurochem. 138:307-316.
Hunsberger, H.C., Konat, G.W. and Reed, M.N. (2017) Peripheral viral challenge elevates extracellular glutamate in the hippocampus leading to seizure hypersusceptibility. J. Neurochem. 141:341-346.
Petrisko, T., Konat, G. (2017) Peripheral viral challenge triggers hippocampal production of inflammatory proteins. Met Brain Dis 32:1249-1254.