Abstract
Voltage-gated ion channels, crucial for maintaining cellular ionic balance, respond to stimuli like changes in membrane voltage potential, influencing the electrical properties of excitable cells such as neurons. Ion selectivity and conduction are central to their functionality, but the precise mechanisms underlying the great efficiency of voltage-gated channels remain only partially understood. In line with this, alternative mechanisms based on quantum coherence have been hypothesised. The hypothesis of quantum coherence playing a role in channel efficiency is tempered by concerns about its compatibility with brain processing time. However, certain neuronal features, such as electromagnetic activity, may extend the duration of these quantum effects. Recent findings highlight the impact of weak electromagnetic fields, akin to the brain's endogenous field, on neuron firing patterns, proposing a central role for calcium homeostasis. In this study, we examined the role in this context of internal calcium release through the endoplasmic reticulum, revealing its key involvement in the cellular effects of electromagnetic fields. As a result, our findings shed light on the modulation of neuronal excitability, particularly in relation to calcium. Additionally, we investigated the effects of weak electromagnetic fields and isotopic exchange, represented by the enrichment of deuterium content, on neuronal membrane currents. Our focus was to explore whether kinetic and magnetic isotopic effects are present. These experimented highlighted a reduction of neuronal excitability upon deuterium enrichment, that was partially rescued by the simultaneous exposure to 1 mT electromagnetic fields at 50 Hz, highlighting the presence of kinetic effects not imputable to mass-dependent effects as viscosity and pH. All together, these experiments describe for the first time an interplay between electromagnetic fields, isotopic variations, and calcium dynamics, providing a more comprehensive understanding of neuronal responses to external stimuli.