Perfect hearing reconstruction necessitates ideal crimping of a prosthesis to obtain consistently good results. However, the final functional gain depends on many different intraoperative and postoperative factors.

The rare finding of round window atresia can be overlooked at surgery because of insufficient exposure of the round window niche. High-resolution computed tomography confirms the round window obliteration. It seems that an alternative way of cochlear stimulation takes place besides the concept of fluid bulk shifting. Surgery seems not to guarantee favorable results.

Probing chemical information in the central nervous system is essential for understanding the molecular mechanism of brain function. Electrochemistry with tissue-implantable carbon fiber electrodes (CFEs) provides a powerful tool for monitoring the dynamics of neurochemicals in a subsecond time scale; however, the implantation of CFEs into brain tissue immediately causes the nonspecific adsorption of proteins on electrode surfaces. This process can dramatically impact the performance of the electrochemical method in terms of reduced sensitivity and accuracy. Herein, we report a strategy to minimize the electrode biofouling by masking CFEs with leukocyte membranes (LMs). We find that the LM masking endows CFEs with a highly hydrophilic surface that gains a high resistance to nonspecific protein adsorption. The electrode reactivity to target molecules decreases by a small degree due to the membrane coating, but the sensitivity loss of the LM-masked CFEs is greatly lessened even after in vivo implantation for 8 h. This study offers a new method of microelectrode modification by natural cell membranes for sustained sensing performance during long-term in vivo analysis.

Neuronal communication relies on cooperation between the chemical and electrical patterns of neurons. Thus, techniques for illustrating the linkage of the neurochemical events and action potentials with high temporal and spatial resolution is imperative to gain a comprehensive understanding of the intricacies of brain function. Herein, we integrate galvanic redox potentiometry (GRP) and electrophysiological recording onto a 16-site Au microelectrode array (MEA), one of which is for indicating the ascorbate concentration while the others for single-unit activity assessment. The electrochemical probing site was modified with single-walled carbon nanotubes to promote electron-transfer kinetics of ascorbate at low overpotential so as to enlarge the driving force for the spontaneous ascorbate/O2 cell reaction. The resulting GRP-based MEA outputs open-circuit potential that is in a linear relationship with the logarithmic ascorbate concentration and exhibits high selectivity against a set of coexisting electroactive species. Furthermore, no reciprocal interference between the two recording systems is observed during concurrent GRP sensing of ascorbate and single-unit recording in a rat brain. In vivo feasibility of the GRP-based MEA is demonstrated by synchronous real-time measurement of ascorbate release and electrical activity from multiple neuronal populations during spreading depression. Our GRP-based MEA sensor creates new opportunities to realize high-throughput screening or mapping of neurochemical patterns in a larger dimension and correlate them to neuron functions across a spatial scale.

Cytotoxic edema is the initial and most important step in the sequence that almost inevitably leads to brain damage. Exploring the neurochemical disturbances in this process is of great significance in providing a measurable biological parameter for signaling specific pathological conditions. Here, we present an electrochemical system that pinpoints a critical neurochemical involved in cytotoxic edema. Specially, we report a molecularly tailored brain-implantable ascorbate sensor (CFE AA2.0 ) featuring excellent selectivity and spatiotemporal resolution that assists the first observation of release of ascorbate induced by cytotoxic edema in vivo. Importantly, we reveal that this release is associated with an increase in the amount of cytotoxic edema-inducing agent and that blockage of cytotoxic edema abolishes ascorbate release, further supporting that ascorbate efflux is cytotoxic edema-dependent. Our study holds the promise for understanding the molecular basis of cytotoxic edema that can lead to the discovery of biomarkers or potential therapeutic strategies of brain diseases.

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