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Full-Text Articles in Nervous System Diseases
Altering Endoplasmic Reticulum Stress In A Model Of Blast-Induced Traumatic Brain Injury Controls Cellular Fate And Ameliorates Neuropsychiatric Symptoms, Aric Flint Logsdon, Ryan Coddington Turner, Brandon Peter Lucke-Wold, Matthew James Robson, Zachary James Naser, Kelly Elizabeth Smith, Rae Reiko Matsumoto
Altering Endoplasmic Reticulum Stress In A Model Of Blast-Induced Traumatic Brain Injury Controls Cellular Fate And Ameliorates Neuropsychiatric Symptoms, Aric Flint Logsdon, Ryan Coddington Turner, Brandon Peter Lucke-Wold, Matthew James Robson, Zachary James Naser, Kelly Elizabeth Smith, Rae Reiko Matsumoto
Faculty Publications & Research of the TUC College of Pharmacy
Neuronal injury following blast-induced traumatic brain injury (bTBI) increases the risk for neuropsychiatric disorders, yet the pathophysiology remains poorly understood. Blood-brain-barrier (BBB) disruption, endoplasmic reticulum (ER) stress, and apoptosis have all been implicated in bTBI. Microvessel compromise is a primary effect of bTBI and is postulated to cause subcellular secondary effects such as ER stress. What remains unclear is how these secondary effects progress to personality disorders in humans exposed to head trauma. To investigate this we exposed male rats to a clinically relevant bTBI model we have recently developed. The study examined initial BBB disruption using Evan’s blue (EB), …