Abstract

Progress has been made in the field of neural interfacing using both mouse and rat models, yet standardization of these models’ interchangeability has yet to be established. The mouse model allows for transgenic, optogenetic, and advanced imaging modalities which can be used to examine the biological impact and failure mechanisms associated with the neural implant itself. The ability to directly compare electrophysiological data between mouse and rat models is crucial for the development and assessment of neural interfaces. The most obvious difference in the two rodent models is size, which raises concern for the role of device-induced tissue strain. Strain exerted on brain tissue by implanted microelectrode arrays is hypothesized to affect long-term recording performance. Therefore, understanding any potential differences in tissue strain caused by differences in the implant to tissue size ratio is crucial for validating the interchangeability of rat and mouse models. Hence, this study is aimed at investigating the electrophysiological variances and predictive device-induced tissue strain. Rat and mouse electrophysiological recordings were collected from implanted animals for eight weeks. A finite element model was utilized to assess the tissue strain from implanted intracortical microelectrodes, taking into account the differences in the depth within the cortex, implantation depth, and electrode geometry between the two models. The rat model demonstrated a larger percentage of channels recording single unit activity and number of units recorded per channel at acute but not chronic time points, relative to the mouse model Additionally, the finite element models also revealed no predictive differences in tissue strain between the two rodent models. Collectively our results show that these two models are comparable after taking into consideration some recommendations to maintain uniform conditions for future studies where direct comparisons of electrophysiological and tissue strain data between the two animal models will be required.

Highlights

  • Intracortical microelectrodes (IMEs) allow for direct interfacing with neuronal populations, thereby enabling the exploration of neuronal function, neurological diseases, and potential therapies (Wise and Angell, 1975; Schwartz, 2004; Kipke et al, 2008)

  • Our evaluation of the rat and mouse models revealed that both have variability within their own animal group, over time, and compared to one another (Figure 2)

  • Electrophysiological Results Electrophysiological recordings from the rat model were compared to the mouse model over the entire course of time, as well as group based on the time course of inflammatory events following device implantation: acute and chronic time points

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Summary

Introduction

Intracortical microelectrodes (IMEs) allow for direct interfacing with neuronal populations, thereby enabling the exploration of neuronal function, neurological diseases, and potential therapies (Wise and Angell, 1975; Schwartz, 2004; Kipke et al, 2008). Intracortical microelectrodes are able to record and transmit electrical impulses directly from neurons in the brain (Renshaw et al, 1940). Recorded electrical impulses can be used in numerous applications, including being translated into control signals for prosthetic devices to restore function (Hochberg et al, 2006; Schwartz et al, 2006; Gilja et al, 2015). The usefulness of IMEs depends on the ability to reliably record the electrical signals from many individual neurons over time (Wise, 2005; Kozai et al, 2015a; Ajiboye et al, 2017). The ability of IMEs to detect isolatable action potentials from individual neurons is directly dependent on the distance between healthy neuronal cell bodies and the microelectrode recording site (Buzsáki, 2004). The complex inflammatory response occurring after electrode implantation results in decreased recording quality within weeks, and a continued decline often leading to complete loss of detectable action potentials within a few years (Chestek et al, 2011; Jorfi et al, 2015; Kozai et al, 2015b)

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