How do neuroglial cells respond to ultrasound induced cavitation?

Reactive astrocytes are known to play a vital role in the overall response of the brain during a traumatic brain injury (TBI). Modern studies have speculated the existence of cavitation in the skull during a TBI, which has alarming potential to cause detrimental damage. Previous studies have confirmed the upregulation of various harmful genes in neurodegenerative diseases. Studying the longitudinal presence of these harmful genes in response to cavitation allows for optimized understanding of and treatment methods for cavitation exposure. We seek to characterize the longitudinal genetic expression levels that astrocytes exhibit after exposure to cavitation and further elucidate the startling presence of cranial cavitation. We have designed a system to induce cavitation on targeted microbubbles. Astrocytic expression levels of various common genes, like TNFα, IL-1β, and NOS1, that have been documented in TBI studies are our target of interest. Results summarize specific gene trends from 1 h to 48 h after cavitation. Our data conclude that maximum expression is not consistently exhibited immediately after cavitation exposure and most genes have individualized genetic trends. IL-1β shows a decreasing expression over 48 h, and TNFα shows upregulation until the 6 h time point but then begins to decrease in expression. The upregulation of NOS1 has been documented in neurodegenerative diseases, like Alzheimer’s and Parkinson’s disease. This study has shown a consistent upregulation in NOS1 expression from 0 h to 48 h. These results postulate a possible linkage between cavitation damage and neurodegenerative diseases. This analysis also provides novelty in optimizing treatments for the astrocytic function after TBI and legitimizing the concern of cranial cavitation existence.