Authors
Fyon, A., Pavlova, O., Schaar, N., Mesirca, P., Brandoit, J., RInglet, S., Franci, A., Mangoni, M. E., Roeper, J., Drion, G., Seutin, V., Jehasse, K.
Abstract
Slow pacemaking is a key physiological process in specific excitable cells, yet its underlying mechanisms remain debated. Here we identify a conserved, voltage-dependent pacemaker current that is essential for slow, regular firing in both midbrain dopaminergic neurons and sinoatrial node cells. Conductance-based models incorporating this current reproduce stable pacemaking, requiring a fast-activating, small-amplitude current. This is further confirmed by dynamic-clamp experiments in dopaminergic neurons. Replacing the pacemaker current in a model with a voltage-independent conductance such as the non-selective sodium leak channels fails to sustain slow rhythmicity, highlighting the necessity for an adequate voltage dependence. Our results suggest a novel and shared biophysical mechanism for slow pacemaking in neuronal and cardiac systems
Preprint server:
bioRxiv
The authors list and abstract were imported from bioRxiv on 31 Oct 2025.
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