- West Virginia University School of Medicine
- West Virginia University WVU Cancer Institute
- WVU Cancer Institute Research Programs
- PhD, University of Southern Denmark
Petrisko, T., Konat, G. (2017) Peripheral viral challenge triggers hippocampal production of inflammatory proteins. Met Brain Dis 32:1249-1254.
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.
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.
Konat, G. (2016) Cerebral response to peripheral challenge with a viral mimetic. Neurochem. Res. 41:144-155.
Michalovicz, L.T., Lally, B. and Konat, G.W. (2015) Peripheral challenge with a viral mimic upregulates expression of the complement genes in the hippocampus. J. Neuroimmunol. 285:137-142.
Salm, A.K., Lally, B.E., Borysiewicz, E., Fil, D. and Konat, G.W. (2015) Analysis of extinction to attenuated tones in prenatally stressed and non-stressed offspring following fear conditioning. Physiol. Behav. 139:157-166.
Michalovicz, L.T. and Konat, G.W. (2014) Peripherally restricted acute phase response to a viral mimic alters hippocampal gene expression. Met. Brain Dis. 29:75-86.
Borysiewicz, E., Doppalapudi S., Kirschman L.T. and Konat, G.W. (2013) TLR3 ligation protects astrocytes against oxidative stress. J. Neuroimmunol. 255:54-59.
Fil, D., Borysiewicz, E. and Konat, G.W. (2011) A broad upregulation of cerebral chemokine genes by peripherally-generated inflammatory mediators. Met. Brain Dis. 26:49-59.
Kirschman, L.T., Fil, D., Borysiewicz, E. and Konat, G.W. (2011) Peripheral immune challenge with dsRNA enhances kainic acid-induced status epilepticus. Met. Brain Dis. 26:91-93.
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.
Metabolic Brain Disease (Editor-in-Chief)
Neurobiology and Anatomy; Center for Basic and Translational Stroke Research
My research interests are primarily focused on the immune-to-brain communication. In particular, the research objective of my laboratory is to elucidate mechanisms by which inflammatory episodes in the periphery alter brain 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 viral infections are comorbid factors in seizures. 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 preclinical murine model in which the peritoneal injection of a viral mimetic, polyinosinic-polycytidylic acid (PIC) robustly increases susceptibility to kainic acid (KA)-induced seizures. Subsequent studies have indicated that the principal mechanism entails dysregulation of glutamate homeostasis in hippocampal astrocytes and that this dysregulation is mediated by the activation of endogenous complement pathways.