Extracellular electrophysiological effects on MEA recordings of living mycelium following in-vivo polydopamine polymerisation

Abstract

Fungi produce multiple melanins found in nature, including the eumelanins (black or dark brown), pheomelanins (yellow or red) and the highly diverse group of allomelanins. The fungal melanins provide protection against UV radiation, oxidative stress, desiccation, host immune evasion and antifungal drug resistance. As a result, research on melanin in fungi is wide ranging including development of anti-fungals and surface interfacing bioelectronics. In-vivo polymerisation of compounds with electrical or ionic conductivity can provide a useful method to interface with the electrophysiology of biological organisms. However, the impact of such interventions is unknown where anti-fungal activity is present and interferes with the target signaling in the organism. Melanin compounds are promising for achieving bioelectronic interfaces with mycelium. However, the identification of the role of melanin in blocking calcium flux in airway epithelial cells and phagosomes underscores the significance of investigating its effects in more detail. Additionally, synthetic analogs such as polydopamine are thought to exhibit similar metal ion chelation properties, supporting the biochemical parallels between natural and artificial melanins. In this paper, we investigate the polymerisation of synthetic melanins in mycelium from the intracellular environment and onto microelectrodes in terms of extracellular electrophysiology. At concentrations of 5 mM and 10 mM extracellular electrophysiological activity is significantly inhibited suggesting a putative link to reduction in Ca2+ efflux and antifungal properties. The dispersed mycelial cultures were estimated to comprise of a total of 200 spiking units across triplicates (T1= 117, T2=40, T3=43). The triplicates had a combined mean trough-to-peak time of 1.72 {+/-} 0.07 ms. Selection of electrophysiology interfacing polymers should be carefully orchestrated to avoid impacting baseline physiology of fungi.