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Abstract
Mild traumatic brain injury is an all-too-common outcome from modern warfare and sport, and lacks a reproducible model for assessment of potential treatments and protection against it. Here we consider the use of surface acoustic wave (SAW) irradiation of C. elegans worms—without cavitation—as a potential, ethically reasonable animal-on-a-chip model for inducing traumatic brain injury in an animal, producing significant effects on memory and learning that could prove useful in a model that progress from youth to old age in but a few weeks. We show a significant effect by SAW on the ability of worms to learn post-exposure through associative learning chemotaxis. At higher SAW intensity, we find immediate, thorough, but temporary paralysis of the worms. We further explore the importance of homogeneous exposure of the worms to the SAW-driven ultrasound, an aspect poorly controlled in past efforts, if at all, and demonstrate the absence of cavitation through a change in fluids from a standard media for the worms to the exceedingly viscous polyvinyl alcohol. Likewise, we demonstrate that acoustic streaming, when present, is not directly responsible for paralysis nor learning disabilities induced in the worm, but is beneficial at low amplitudes to ensuring homogeneous ultrasound exposure.
Highlights
Bi-mTBI—the least understood damage mechanism caused by exposure to the primary blast wave27—may not show diagnostic signs of injury while still leading to serious long-term consequences[11,28,29,30,31,32]
In this study, and beyond past reports showing paralysis and morphological changes, we show how exposure to high frequency acoustic waves generated by our surface acoustic wave (SAW) apparatus can affect C. elegans in two ways analogous to bi-mTBI observed in humans and mammals: reduction of both mobility and short-term memory
The dose-dependent mobility of C. elegans was studied for several SAW power levels and different exposure durations, from 5 s to 10 min, and an exposure time of 10 s was chosen as a balance between reducing any risk of heating effects and sufficient time for effects to arise from the SAW on the mobility of the worms
Summary
Bi-mTBI—the least understood damage mechanism caused by exposure to the primary blast wave27—may not show diagnostic signs of injury while still leading to serious long-term consequences[11,28,29,30,31,32]. This may be the reason that a significant number of clinical drug trials fail after seeing potential preclinical benefit with blast injury exposure testing[42] All of these models require significant preparation time and the requisite ethics approvals, and are expensive to employ given the large number of animals required to discern biologically relevant effects, the protracted effort necessary to perform behavioral tests, and generally low throughput. These problems collectively limit progress in the pursuit of better treatment. We use C. elegans in this study as an alternative model organism to vertebrate animals (e.g., mice, rats, pigs)
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