Seminars in Hearing Research at Purdue (SHRP)

Title: Mechanisms of Secondary Injury and Auditory Deficits Following Mild Blast Induced Trauma

Authors:

Joseph Fernandez [1,4], Emily Han [1], Edward Bartlett [1,3], Riyi Shi [1,3,4]

[1] Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN

[2] School of Medicine, Indiana University, Indianapolis, IN

[3] Purdue University Interdisciplinary Life Science (PULSe) Program, Purdue University, West Lafayette, IN

[4] Dept. Basic Medical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN

Speaker: Joseph Fernandez, Ph.D. Student, BME

Date: April 29, 2021

Time: 10:30 – 11:20 am

Zoom Info:

https://purdue-edu.zoom.us/j/98209787906?pwd=YnZCcy9ucnlJZE5IQmxBMzBBSmY5Zz09

Meeting ID: 982 0978 7906

Passcode: 064752

Abstract:

Blast-induced hearing difficulties affect thousands of veterans and civilians each year. The long-term impact of blast exposure on the central auditory system (CAS) can last months, even years, without major external injury, and is hypothesized to contribute to many behavioral complaints associated with mild blast traumatic brain injury (bTBI). However, the mechanisms that underlie these long-term impairments are still poorly understood. Examining the acute time course and pattern of neurophysiological impairment (within the first two weeks), as well as the underlying molecular and anatomical post injury environment is therefore critical to understanding the mechanisms that lead to long-term CAS impairments. Although initial mechanical injury likely plays a role in central auditory damage, a secondary molecular mechanism of damage likely results in the chronic auditory deficits following mild bTBI. Oxidative stress, along with inflammation, have been suggested as key players in secondary molecular damage in other models of CNS injury, including other TBIs, and may underlie functional auditory deficits in mild bTBI as well. Here, we recorded the changes in a variety auditory evoked potential (AEPs) in blast-exposed and noise-control rats over the course of two months to understand regionally and temporal specific deficits. We compared these results to molecular and anatomical changes observed in immunohistochemistry staining, to understand the relationship between AEP and anatomical changes. Taken together, our results suggest that an acute cascade of (axonal) membrane damage and oxidative stress results in a temporally dependent inhibition/excitation imbalance over the course of two weeks.

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The working schedule is available here:

https://purdue.edu/TPAN/hearing/shrp_schedule

The titles and abstracts of the talks will be added here:

https://purdue.edu/TPAN/hearing/shrp_abstracts