Abstract
Microelectrode arrays (MEAs) provide promising opportunities to study electrical signals in neuronal and cardiac cell networks, restore sensory function, or treat disorders of the nervous system. Nevertheless, most of the currently investigated devices rely on silicon or polymer materials, which neither physically mimic nor mechanically match the structure of living tissue, causing inflammatory response or loss of functionality. Here, we present a new method for developing soft MEAs as bioelectronic interfaces. The functional structures are directly deposited on PDMS-, agarose-, and gelatin-based substrates using ink-jet printing as a patterning tool. We demonstrate the versatility of this approach by printing high-resolution carbon MEAs on PDMS and hydrogels. The soft MEAs are used for in vitro extracellular recording of action potentials from cardiomyocyte-like HL-1 cells. Our results represent an important step toward the design of next-generation bioelectronic interfaces in a rapid prototyping approach.
Highlights
Printed soft Microelectrode arrays (MEAs) arrays passivation films is dewetting, which is especially important for covering areas that are larger than two printed drops.[87]
12 mm[2] substrate. b Step 2: inner feedlines and MEAs are printed with carbon nanoparticle ink. c Step 3: A 9 × 9 mm[2] passivation layer is printed with polyimide ink (PI). d–f Microscopic images of the successive printing process of a carbon MEA on PDMS subsequently depositing d silver ink, e carbon ink, and f PI ink
We demonstrated the development and application of printed MEA arrays on soft substrates including PDMS and hydrogels
Summary
Microelectrode arrays (MEAs) have attracted strong interest due to their use in various applications, including cellular recording, biosensors, and drug screening.[1,2,3,4,5,6,7,8,9,10,11] Perhaps one of the most promising application of MEA devices are biomedical implants in which the MEA serves as a vital tool for monitoring or restoring biological functionality.[12,13,14] Historically, MEA devices, as developed by Wise and co-worker[15] in the late 1960s, consisted of conductive metallic material covered by an insulating layer, except for a small electrode opening to establish a connection to the surrounding tissue. The stiff substrate alters cell shape, organization, and function and does not represent a model close to the natural cellular behavior with soft surrounding tissue.[27,28,29,30] In vivo, the stiff synthetic substrate may trigger inflammatory response or loss of functionalities, indicating rejection of the electronic interface and precluding successful translation of these probes to clinical research.20,2331,32 rigid electronic implants can alter the physiological movement of organs such as the heart[33,34,35] and neuronal tissue.[36,37,38]
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