Annalisa Bucchi

TL;DR: A comparison of four isoforms of hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels have been cloned more recently and shown to be the molecular correlates of native f-channels in the heart and h-ch channels in the brain, providing insight into the molecular basis of the pacemaker current properties.

TL;DR: The data suggest that permeation through f-channel pores occurs according to a multiion, single-file mechanism, and that block/unblock by ivabradine is coupled to ionic flow, a feature typical of block induced in inwardly rectifying K+ channels by intracellular cations.

TL;DR: The data show that cardiac HCN 4 channels are essential for normal heart impulse generation and conduction in adult mice and support the notion that dysfunctional HCN4 channels can be a direct cause of rhythm disorders.

TL;DR: It is demonstrated that training-induced bradycardia persists after blockade of the autonomous nervous system in vivo in mice and in vitro in the denervated sinus node, providing a molecular explanation for the potentially pathological heart rate adaptation to exercise training.

TL;DR: It is found that bath application of exogenous PI(4,5)P2 reverses the effect of rundown, producing a large depolarizing shift in HCN2 activation, and both native and recombinant HCN channels are regulated by PI( 4,5), although phosphatidylinositol (PI) is ineffective.