IBSC-BME PhD Preliminary Exam Announcement for Jhon Martinez (R. Shi, advisor) Everyone is invited to attend the public presentation beginning at 3:00 pm. Title: Mechanistic Insights into Neuroprotective Strategies: Studying Neuronal Network Activity Changes in an In Vitro Model of Blast-Induced TBI Date: Thursday, November 19 Time: 3:00 pm Location: MJIS 2001and Zoom https://purdue-edu.zoom.us/j/3867778660?omn=94227865837<https://nam04.safelinks.protection.outlook.com/?url=https%3A%2F%2Fpurdue-edu.zoom.us%2Fj%2F3867778660%3Fomn%3D94227865837&data=05%7C02%7Cbmeroundtable-list%40ecn.purdue.edu%7C91bcfd497fe04103815a08dcfeacf7c3%7C4130bd397c53419cb1e58758d6d63f21%7C0%7C0%7C638665266041996686%7CUnknown%7CTWFpbGZsb3d8eyJFbXB0eU1hcGkiOnRydWUsIlYiOiIwLjAuMDAwMCIsIlAiOiJXaW4zMiIsIkFOIjoiTWFpbCIsIldUIjoyfQ%3D%3D%7C0%7C%7C%7C&sdata=DFOiuOUQZ0NaItq3AVYoEd6dsHB%2BMxgTyAFoBgVckVE%3D&reserved=0> Committee Members: Riyi Shi (chair), Charles Babbs, Bradley Duerstock, and Ranjie Xu Abstract: Traumatic brain injury (TBI) is a significant global public health issue, affecting up to 74 million individuals each year. In war zones, individuals are particularly vulnerable to Blast-Induced Traumatic Brain Injury (bTBI), which can result from exposure to explosive shockwaves. After the initial injury (primary injury), chemical cascades and chronic brain inflammation can further spread damage (secondary injury). Both primary and secondary injury can trigger long-term behavioral and cognitive deficiencies, including an increased risk of neurodegenerative diseases. These changes can occur even for mild injuries (mbTBI), where immediate symptoms may not be apparent. Key components of secondary injury that contribute to long-term brain pathology are oxidative stress, elevated levels of reactive oxygen species (ROS), and increased levels of acrolein. In particular, acrolein is a highly reactive aldehyde that plays a central role in exacerbating cellular damage. However, the link between cellular damage and brain pathologies remains unclear and requires a better understanding of how damage alters cell function at the cellular and sub-cellular levels. This study aims to investigate injury-related changes at the cellular level using a TBI-on-a-chip model, in which primary murine cortical neuronal networks are cultured on microelectrode arrays (MEAs), allowing recordings of neuronal activity (spikes) before and after mbTBI administration. We observed that mbTBI led to immediate functional alterations, including reduced spike rate and alterations to bursts (coordinated activity with rapid spiking) patterns, such as reduced burst rate, burst duration, and an increase in burst period. Additionally, cross-correlation analysis of MEA recordings revealed disruptions in firing order dynamics, with notable changes in firing hierarchy and the number of correlogram peaks, indicating altered temporal coordination between neurons. Furthermore, employing acrolein-scavenging drugs, such as hydralazine, helped restore aspects of network function, suggesting that neutralizing acrolein may mitigate mbTBI-induced deficits. These findings indicate that mbTBI significantly alters neuronal firing, potentially contributing to neurodegeneration, and that targeting secondary injury mechanisms, such as acrolein scavenging, could help preserve neuronal integrity and function. -- Bmeroundtable-list mailing list Bmeroundtable-list@ecn.purdue.edu https://engineering.purdue.edu/ECN/mailman/listinfo/bmeroundtable-list