Three-dimensional (3D) movement of neuroprosthetic devices can be controlled by the activity of cortical neurons when appropriate algorithms are used to decode intended movement in real time. Previous studies assumed that neurons maintain fixed tuning properties, and the studies used subjects who were unaware of the movements predicted by their recorded units. In this study, subjects had real-time visual feedback of their brain-controlled trajectories. Cell tuning properties changed when used for brain-controlled movements. By using control algorithms that track these changes, subjects made long sequences of 3D movements using far fewer cortical units than expected. Daily practice improved movement accuracy and the directional tuning of these units.
Microwire electrode arrays were implanted in the motor and premotor cortical areas of rhesus macaques. The recorded activity was used to control the three-dimensional movements of a virtual cursor and of a robotic arm in real time. The goal was to move the cursor or robot to one of eight targets. Average information conveyed about the intended target was calculated from the observed trajectories at 30-ms intervals throughout the movements. Most of the information about intended target was conveyed within the first second of the movement. For the brain-controlled cursor, the instantaneous information transmission rate was at its maximum at the beginning of each movement (averaged 4.8 to 5.5 bits/s depending on the calculation method used). However, this instantaneous rate quickly slowed down as the movement progressed and additional information became redundant. Information was conveyed more slowly through the brain-controlled robot due to the dynamics and noise of the robot system. The brain-controlled cursor data was also used to demonstrate a method for optimizing information transmission rate in the case where repeated cursor movements are used to make long strings of sequential choices such as in a typing task.
Intracortical microelectrodes afford researchers an effective tool to precisely monitor neural spiking activity. Additionally, intracortical microelectrodes have the ability to return function to individuals with paralysis as part of a brain computer interface. Unfortunately, the neural signals recorded by these electrodes degrade over time. Many strategies which target the biological and/or materials mediating failure modes of this decline of function are currently under investigation. The goal of this study is to identify a precise cellular target for future intervention to sustain chronic intracortical microelectrode performance. Previous work from our lab has indicated that the Cluster of Differentiation 14/Toll-like receptor pathway (CD14/TLR) is a viable target to improve chronic laminar, silicon intracortical microelectrode recordings. Here, we use a mouse bone marrow chimera model to selectively knockout CD14, an innate immune receptor, from either brain resident microglia or blood-derived macrophages, in order to understand the most effective targets for future therapeutic options. Using single-unit recordings we demonstrate that inhibiting CD14 from the blood-derived macrophages improves recording quality over the 16 week long study. We conclude that targeting CD14 in blood-derived cells should be part of the strategy to improve the performance of intracortical microelectrodes, and that the daunting task of delivering therapeutics across the blood-brain barrier may not be needed to increase intracortical microelectrode performance.
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