Information processing in the mammalian brain relies on a careful regulation of the membrane potential dynamics of its constituent neurons, which propagates across the neuronal tissue via electrical signalling. We recently reported the existence of electrical signalling in a much simpler organism, the bacterium Bacillus subtilis. In dense bacterial communities known as biofilms, nutrient-deprived B. subtilis cells in the interior of the colony use electrical communication to transmit stress signals to the periphery, which interfere with the growth of peripheral cells and reduce nutrient consumption, thereby relieving stress from the interior. Here, we explicitly address the interplay between metabolism and electrophysiology in bacterial biofilms, by introducing a spatially extended mathematical model that combines the metabolic and electrical components of the phenomenon in a discretized reaction-diffusion scheme. The model is experimentally validated by environmental and genetic perturbations, and confirms that metabolic stress is transmitted through the bacterial population via a potassium wave. Interestingly, this behaviour is reminiscent of cortical spreading depression in the brain, characterized by a wave of electrical activity mediated by potassium diffusion that has been linked to various neurological disorders, calling for future studies on the evolutionary link between the two phenomena. This article is part of the theme issue 'Liquid brains, solid brains: How distributed cognitive architectures process information'.

This work was supported by the Spanish Ministry of Economy and Competitiveness and FEDER (project FIS2015-66503-C3-1-P), and by the Generalitat de Catalunya (project 2017 SGR 1054). R.M.C. acknowledges financial support from La Caixa foundation. J.G.O. acknowledges support from the ICREA Academia programme and from the “Mar ́ıa de Maeztu” Programme for Units of Excellence in R&D (Spanish Ministry of Economy and Competitiveness, MDM-2014-0370). G.M.S. acknowledges support for this research from the San Diego Center for Systems Biology (NIH grant P50 GM085764), the National Institute of General Medical Sciences (grant R01 GM121888), the Defense Advanced Research Projects Agency (grant HR0011-16-2-0035), and the Howard Hughes Medical Institute-Simons Foundation Faculty Scholars program. A.P. is supported by a Simons Foundation Fellowship of the Helen Hay Whitney Foundation and a Career Award at the Scientific Interface from the Burroughs Wellcome Fund.