Title: A modular, adaptable, and accessible implant kit for chronic electrophysiological recordings in rats
Electrophysiological implants enable exploration of the relationship between neuronal activity and behavior. These technologies evolve rapidly, with multiple iterations of recording systems developed and utilized. Chronic implants must address a litany of complications, including retention of high signal-to-noise ratio in probes and the ability to withstand excess force over the experimental period. To overcome these issues, we designed a chronic implant for rats. Our comprehensive protocol optimizes the entire implant process, from assembling and testing the probes (Neuropixels) to implantation. In addition to addressing the complications previously mentioned, our implant can vertically adjust probes with micron precision and is constructed using modular components, allowing it to be easily modified for various research contexts, electrophysiological recording systems, headstages, and probe types. more »« less
Ibáñez_Alcalá, Raquel J; Macias, Andrea Y; Heaton, Cory N; Sosa_Jurado, Ricardo; Salcido, Alexis A; Reyes, Neftali F; Batson, Serina A; Davila, Luis D; Beck, Dirk W; Rakocevic, Lara I; et al
(, Cell Reports Methods)
Electrophysiological implants enable exploration of the relationship between neuronal activity and behavior. These technologies evolve rapidly, with multiple iterations of recording systems developed and utilized. Chronic implants must address a litany of complications, including retention of high signal-to-noise ratio in probes and the ability to withstand excess force over the experimental period. To overcome these issues, we designed a chronic implant for rats. Our comprehensive protocol optimizes the entire implant process, from assembling and testing the probes (Neuropixels) to implantation. In addition to addressing the complications previously mentioned, our implant can vertically adjust probes with micron precision and is con- structed using modular components, allowing it to be easily modified for various research contexts, electro- physiological recording systems, headstages, and probe types.
Rosas, Jonah M.; Atkins, Dixon J.; Chau, Allison L.; Chen, Yen-Tsung; Bae, Rachel; Cavanaugh, Megan K.; Espinosa Lima, Ricardo I.; Bordeos, Andrew; Bryant, Michael G.; Pitenis, Angela A.
(, Proceedings of the Institution of Mechanical Engineers, Part J: Journal of Engineering Tribology)
Silicone elastomer medical implants are ubiquitous in medicine, particularly for breast augmentation. However, when these devices are placed within the body, disruption of the natural biological interfaces occurs, which significantly changes the native energy-dissipation mechanisms of living systems. These new interfaces can introduce non-physiological contact pressures and tribological conditions that provoke inflammation and soft tissue damage. Despite their significance, the biotribological properties of implant-tissue and implant-extracellular matrix (ECM) interfaces remain poorly understood. Here, we developed an in vitro model of soft tissue damage using a custom-built in situ biotribometer mounted onto a confocal microscope. Sections of commercially-available silicone breast implants with distinct and clinically relevant surface roughness ([Formula: see text]m, [Formula: see text]m, and [Formula: see text]m) were mounted to spherically-capped hydrogel probes and slid against collagen-coated hydrogel surfaces as well as healthy breast epithelial (MCF10A) cell monolayers to model implant-ECM and implant-tissue interfaces. In contrast to the “smooth” silicone implants ([Formula: see text]m), we demonstrate that the “microtextured” silicone implant ([Formula: see text]m) induced higher frictional shear stress ([Formula: see text] Pa), which led to greater collagen removal and cell rupture/delamination. Our studies may provide insights into post-implantation tribological interactions between silicone breast implants and soft tissues.
Intracortical microelectrodes have become a useful tool in neuroprosthetic applications in the clinic and to understand neurological disorders in basic neurosciences. Many of these brain-machine interface technology applications require successful long-term implantation with high stability and sensitivity. However, the intrinsic tissue reaction caused by implantation remains a major failure mechanism causing loss of recorded signal quality over time. Oligodendrocytes remain an underappreciated intervention target to improve chronic recording performance. These cells can accelerate action potential propagation and provides direct metabolic support for neuronal health and functionality. However, implantation injury causes oligodendrocyte degeneration and leads to progressive demyelination in surrounding brain tissue. Previous work highlighted that healthy oligodendrocytes are necessary for greater electrophysiological recording performance and the prevention of neuronal silencing around implanted microelectrodes over the chronic implantation period. Thus, we hypothesize that enhancing oligodendrocyte activity with a pharmaceutical drug, Clemastine, will prevent the chronic decline of microelectrode recording performance. Electrophysiological evaluation showed that the promyelination Clemastine treatment significantly elevated the signal detectability and quality, rescued the loss of multi-unit activity, and increased functional interlaminar connectivity over 16-weeks of implantation. Additionally, post-mortem immunohistochemistry showed that increased oligodendrocyte density and myelination coincided with increased survival of both excitatory and inhibitory neurons near the implant. Overall, we showed a positive relationship between enhanced oligodendrocyte activity and neuronal health and functionality near the chronically implanted microelectrode. This study shows that therapeutic strategy that enhance oligodendrocyte activity is effective for integrating the functional device interface with brain tissue over chronic implantation period.
Danila, Delia; Pardo, Patricia S; Misra, R_Devesh Kumar; Boriek, Aladin M
(, Current issues in molecular biology)
Liposomes are tiny, spherical vesicles made from cholesterol and natural phospholipids that are promising imaging agents for detecting medical complications. They can carry fluorescent markers or other imaging agents, making them effective for medical imaging. Furthermore, liposomes can target specific cells involved in inflammation, such as macrophages, and accumulate at inflammation sites when injected. Additionally, liposomes can be designed to respond to oxidative stress, which is often associated with bone implant complications. By detecting areas of stress, liposomes provide valuable information about implant health. However, challenges such as rapid clearance from the body, precise targeting, immune reactions, and high production costs must be addressed. Research is ongoing to improve the design and functionality of liposomes. They can potentially monitor bone implants as non-invasive imaging agents, enabling early detection of complications and timely interventions. This approach can enhance patient outcomes and extend the longevity of implants, making it a promising strategy for better patient care and implant success.
Macrotextured silicone breast implants are associated with several complications, ranging from seromas and hematomas to the formation of a rare type of lymphoma, known as breast implant-associated anaplastic large cell lymphoma (BIA-ALCL). The presence of silicone wear debris has been detected within the peri-implant region and fibrotic capsule and histological analyses reveal inflammatory cells surrounding debris particles. However, it is unclear how these debris particles are generated and released from macrotextured implant surfaces, and whether wear debris generation is related to implant stiffness. In this study, we created an accelerated implant aging model to investigate the formation of silicone wear debris produced from self-mated (“shell-shell”) tribological interactions. We created implant-like silicone elastomers from polydimethylsiloxane (PDMS) using Sylgard 184 base:curing agent (10:1, 12:1, and 16:1) and quantified their mechanical properties E* = 1141 ± 472, 336 ± 20, and 167 ± 53 kPa, respectively). We created macrotextured PDMS samples using the lost-salt technique and compared their self-mated friction coefficient µ = 4.8 ± 3.2, 4.9 ± 1.8, and 6.0 ± 2.3, respectively) and frictional shear stress (τ = 3.1 ± 1.3, 3.2 ± 1.7, and 2.4 ± 1.4 MPa, respectively) to those of the recalled Allergan Biocell macrotextured implant shell (E* = 299 ± 8 kPa, µ = 2.2, and τ = 0.8 ± 0.1). Friction coefficient and frictional shear stress were largely insensitive to variations in elastic modulus for macrotextured PDMS samples and recalled implant shells. The stiffest 10:1 PDMS macrotextured sample and the recalled implant shell both generated similar area fractions of silicone wear debris. However, the recalled implant shell released far more particles (> 10×), mainly within the range of 5 to 20 µm squared in area. Bone marrow-derived macrophages (BMDMs) were treated with several concentrations of tribologically generated silicone wear debris. We observed widespread phagocytosis of wear debris particles and increasing secretion of inflammatory cytokines with increasing concentration of wear debris particles. Our investigation highlights the importance of avoiding macrotextured surfaces and mitigating wear debris generation from silicone implants to reduce chronic inflammation.
Ibanez-Alcala, RJ, Macias, AY, Heaton, CN, Sosa-Jurado, R, Salcido, AA, Reyes, NF, Batson, SA, Davila, LD, Beck, DW, Rakocevic, LI, Giri, A, Negishi, K, Drammis, S M, Goosens, KA, Moschak, TM, and Friedman, A. A modular, adaptable, and accessible implant kit for chronic electrophysiological recordings in rats. Retrieved from https://par.nsf.gov/biblio/10679816. Cell Reports Methods 5.9
Ibanez-Alcala, RJ, Macias, AY, Heaton, CN, Sosa-Jurado, R, Salcido, AA, Reyes, NF, Batson, SA, Davila, LD, Beck, DW, Rakocevic, LI, Giri, A, Negishi, K, Drammis, S M, Goosens, KA, Moschak, TM, & Friedman, A. A modular, adaptable, and accessible implant kit for chronic electrophysiological recordings in rats. Cell Reports Methods, 5 (9). Retrieved from https://par.nsf.gov/biblio/10679816.
Ibanez-Alcala, RJ, Macias, AY, Heaton, CN, Sosa-Jurado, R, Salcido, AA, Reyes, NF, Batson, SA, Davila, LD, Beck, DW, Rakocevic, LI, Giri, A, Negishi, K, Drammis, S M, Goosens, KA, Moschak, TM, and Friedman, A.
"A modular, adaptable, and accessible implant kit for chronic electrophysiological recordings in rats". Cell Reports Methods 5 (9). Country unknown/Code not available: Cell Reports Methods. https://par.nsf.gov/biblio/10679816.
@article{osti_10679816,
place = {Country unknown/Code not available},
title = {A modular, adaptable, and accessible implant kit for chronic electrophysiological recordings in rats},
url = {https://par.nsf.gov/biblio/10679816},
abstractNote = {Electrophysiological implants enable exploration of the relationship between neuronal activity and behavior. These technologies evolve rapidly, with multiple iterations of recording systems developed and utilized. Chronic implants must address a litany of complications, including retention of high signal-to-noise ratio in probes and the ability to withstand excess force over the experimental period. To overcome these issues, we designed a chronic implant for rats. Our comprehensive protocol optimizes the entire implant process, from assembling and testing the probes (Neuropixels) to implantation. In addition to addressing the complications previously mentioned, our implant can vertically adjust probes with micron precision and is constructed using modular components, allowing it to be easily modified for various research contexts, electrophysiological recording systems, headstages, and probe types.},
journal = {Cell Reports Methods},
volume = {5},
number = {9},
publisher = {Cell Reports Methods},
author = {Ibanez-Alcala, RJ and Macias, AY and Heaton, CN and Sosa-Jurado, R and Salcido, AA and Reyes, NF and Batson, SA and Davila, LD and Beck, DW and Rakocevic, LI and Giri, A and Negishi, K and Drammis, S M and Goosens, KA and Moschak, TM and Friedman, A},
}
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