Voltage based spike-timing dependent myelin plasticity

Abstract

There is an increasing body of evidence from both in vivo studies (Varela et al., 2001; Wang, 2010; Siegel, Donner, & Engel, 2010) and simulated networks (Izhikevich & Edelman, 2008; Noori et al. 2020) that the brain's processing requires synchronization of spike arrival times. One of the most promising mechanisms suggested to meet this requirement is compensating myelination, where adaptive levels of myelin insulation reduce longer conduction delays to synchronize with shorter ones (Salami et al., 2003; Vicente et al., 2008; Seidl, 2014). This compensation is produced through homeostatic regulation of myelin levels, converging onto a particular level of myelin for a given phase-locked pattern of stimulation (Domingues et al. 2016, Noori et al. 2020). We introduce a plausible biological mechanism for the regulation of activity dependent myelin plasticity, and a computational model of this mechanism which ultimately produces stable, homeostatic dynamics analogous to voltage-based STDP models. Our model synchronizes coherently out-of-phase inputs via changes in conduction velocity, and makes predictions about the proteins, neurotransmitters, and ions involved in adaptive CNS myelin plasticity.