Regulation of XOR function of reduced human L2/3 pyramidal neurons

Abstract

The apical dendrites of human L2/3 pyramidal neurons are capable of performing XOR computation by modulating the amplitude of dendritic calcium action potentials (dCaAPs) mediated by calcium ions. What influences this particular function? There is still no answer to this question. In this study, we employed a rational and feasible reduction method to successfully derive simplified models of human L2/3 pyramidal neurons while preserving their detailed functional properties. Using a conductance-based model, we manipulated the membrane potential of the apical dendrite in the simplified model. Our findings indicate that an increase in sodium conductance (\({g}_{Na}\)) and membrane capacitance (\({C}_{m}\)) weakens the XOR function, while regulation of potassium conductance (\({g}_{K}\)) demonstrates robustness in maintaining the XOR function. Further analysis reveals that when a single pathway is activated, an increase in \({g}_{Na}\) and \({C}_{m}\) leads to decrease in the amplitude of dCaAPs, whereas increasing \({g}_{K}\) has a relatively minor impact on dCaAPs amplitude. In conclusion, although calcium ions play a crucial role in enabling apical dendrites of human L2/3 pyramidal neurons to perform XOR computation, other ion channels’ conductance and membrane capacitance can also influence this function.