Implantable microelectrode arrays (MEAs) enable the recording of electrical activity of cortical neurons, allowing the development of brain-machine interfaces. However, MEAs show reduced recording capabilities under chronic conditions, prompting the development of novel MEAs that can improve long-term performance. Conventional planar, silicon-based devices and ultra-thin amorphous silicon carbide (a-SiC) MEAs were implanted in the motor cortex of female Sprague–Dawley rats, and weekly anesthetized recordings were made for 16 weeks after implantation. The spectral density and bandpower between 1 and 500 Hz of recordings were compared over the implantation period for both device types. Initially, the bandpower of the a-SiC devices and standard MEAs was comparable. However, the standard MEAs showed a consistent decline in both bandpower and power spectral density throughout the 16 weeks post-implantation, whereas the a-SiC MEAs showed substantially more stable performance. These differences in bandpower and spectral density between standard and a-SiC MEAs were statistically significant from week 6 post-implantation until the end of the study at 16 weeks. These results support the use of ultra-thin a-SiC MEAs to develop chronic, reliable brain-machine interfaces.

Implantable microelectrode arrays (MEAs) enable the recording of electrical activity from cortical neurons for applications that include brain–machine interfaces. However, MEAs show reduced recording capabilities under chronic implantation conditions. This has largely been attributed to the brain’s foreign body response, which is marked by neuroinflammation and gliosis in the immediate vicinity of the MEA implantation site. This has prompted the development of novel MEAs with either coatings or architectures that aim to reduce the tissue response. The present study examines the comparative performance of multi-shank planar, silicon-based devices and low-flexural-rigidity amorphous silicon carbide (a-SiC) MEAs that have a similar architecture but differ with respect to the shank cross-sectional area. Data from a-SiC arrays were previously reported in a prior study from our group. In a manner consistent with the prior work, larger cross-sectional area silicon-based arrays were implanted in the motor cortex of female Sprague-Dawley rats and weekly recordings were made for 16 weeks after implantation. Single unit metrics from the recordings were compared over the implantation period between the device types. Overall, the expression of single units measured from a-SiC devices was significantly higher than for silicon-based MEAs throughout the implantation period. Immunohistochemical analysis demonstrated reduced neuroinflammation and gliosis around the a-SiC MEAs compared to silicon-based devices. Our findings demonstrate that the a-SiC MEAs with a smaller shank cross-sectional area can record single unit activity with more stability and exhibit a reduced inflammatory response compared to the silicon-based device employed in this study.

PIEZO1 is a mechanosensitive ion channel expressed in various organs, including but not limited to the brain, heart, lungs, kidneys, bone, and skin. PIEZO1 has been implicated in astrocyte, microglia, capillary, and oligodendrocyte signaling in the mammalian cortex. Using murine embryonic frontal cortex tissue, we examined the protein expression and functionality of PIEZO1 channels in cultured networks leveraging substrate-integrated microelectrode arrays (MEAs) with additional quantitative results from calcium imaging and whole-cell patch-clamp electrophysiology. MEA data show that the PIEZO1 agonist Yoda1 transiently enhances the mean firing rate (MFR) of single units, while the PIEZO1 antagonist GsMTx4 inhibits both spontaneous activity and Yoda1-induced increase in MFR in cortical networks. Furthermore, calcium imaging experiments revealed that Yoda1 significantly increased the frequency of calcium transients in cortical cells. Additionally, in voltage clamp experiments, Yoda1 exposure shifted the cellular reversal potential towards depolarized potentials consistent with the behavior of PIEZO1 as a non-specific cation-permeable channel. Our work demonstrates that murine frontal cortical neurons express functional PIEZO1 channels and quantifies the electrophysiological effects of channel activation in vitro. By quantifying the electrophysiological effects of PIEZO1 activation in vitro, our study establishes a foundation for future investigations into the role of PIEZO1 in neurological processes and potential therapeutic applications targeting mechanosensitive channels in various physiological contexts.

Intracortical microelectrode arrays (MEAs) are tools for recording and stimulating neural activity, with potential applications in prosthetic control and treatment of neurological disorders. However, when chronically implanted, the long-term functionality of MEAs is hindered by the foreign body response (FBR), characterized by gliosis, neuronal loss, and the formation of a glial scar encapsulating layer. This response begins immediately after implantation and is exacerbated by factors such as brain micromotion and the mechanical mismatch between stiff electrodes and soft brain tissue, leading to signal degradation. Despite progress in mitigating these issues, the underlying mechanisms of the brain’s response to MEA implantation remain unclear, particularly regarding how cells sense and respond to the associated mechanical forces. Mechanosensitive ion channels, such as the Piezo family, are key mediators of cellular responses to mechanical stimuli. In this study, silicon-based NeuroNexus MEAs consisting of four shanks were implanted in the rat somatosensory cortex for sixteen weeks. Weekly neural recordings were conducted to assess signal quality over time, revealing a decline in active electrode yield and signal amplitude. Immunohistochemical analysis showed an increase in GFAP intensity and decreased neuronal density near the implant site. Furthermore, Piezo1—but not Piezo2—was strongly expressed in GFAP-positive astrocytes within 25 µm of the implant. Piezo2 expression appeared relatively uniform within each brain slice, both in and around the MEA implantation site across cortical layers. Our study builds on previous work by demonstrating a potential role of Piezo1 in the chronic FBR induced by MEA implantation over a 16-week period. Our findings highlight Piezo1 as the primary mechanosensitive channel driving chronic FBR, suggesting it may be a target for improving MEA design and long-term functionality.

This study reveals that locomotion speed is encoded in mouse primary motor cortex through a sigmoidal state-transition mechanism carried by two functionally distinct spiking populations with a shared speed threshold. Using high-density laminar recordings and markerless motion tracking, we show that this framework extends to local field potentials and enables accurate, generalizable decoding. These findings establish a push-pull sigmoidal architecture and highlight implications for stable, calibration-light brain-machine interface design.