 Hyperpolarized activated and cyclic nucleotide gated, HCN, channels are the only members of the voltage gated ion channel superfamily in mammals that open upon hyperpolarization, confaring them pacemaker properties that are instrumental for rhythmic firing of cardiac and neuronal cells. Activation of their voltage sensor domains, VSD, upon hyperpolarization occurs through a downward movement of the S4 helix bearing the gating charges, which triggers a break in the alpha helical hydrogen bonding pattern at the level of a conserved serine residue. Previous structural and molecular simulation studies had however failed to capture poor opening that should be triggered by VSD activation, presumably because of a low VSD poor electromechanical coupling efficiency and the limited timescales accessible to such techniques. Here, we have used advanced modeling strategies, including enhanced sampling molecular dynamic simulations exploiting comparisons between non-domain swapped voltage gated ion channel structures trapped in closed and open states to trigger poor gating and characterize electromechanical coupling in HCN1. We propose that the coupling. This article was authored by Ahmed Ilbansi, John Cowgill, Verena Bertscher, and others. We are article.tv, links in the description below.