Modelling ionic channels represents a fundamental step towards developing biologically detailed neuron models. Until recently, the voltage-gated ion channels have been mainly modelled according to the formalism introduced by the seminal works of Hodgkin and Huxley (HH). However, following the continuing achievements in the biophysical and molecular comprehension of these pore-forming transmembr...

Voltage-gated Na+ channels (VGSC) are transmembrane proteins that are essential for the initiation and propagation of action potentials in neuronal excitability. Because neurons express a mixture of Na+ channel isoforms and protein kinase C (PKC) isozymes, the nature of which channel is being regulated by which PKC isozyme is not known. We showed that DRG VGSC Nav1.7 (TTX-sensitive) and Nav1.8 ...

Voltage-gated sodium channels are responsible for excitable cell action potential initiation. In cardiomyocytes, SCN5A-encoded Nav1.5 is the primary voltage-gated sodium channel a subunit, although other Nav channel a subunits may secondarily modulate specific INa properties. In addition to the pore-forming Nav1.5 a subunits, four accessory Nav b subunits (b1–b4) are expressed in the human hear...

Background: Auxiliary  subunits regulate the voltage-gated sodium channels of DRG neurons. Results:  subunits are differentially expressed in subpopulations of DRG neurons and regulate Nav1.7 channels in an isoform-specific manor. Conclusions: Differential  subunit expression and isoform-specific regulation has important implications for the sodium currents of DRG neurons. Significance:  su...

Voltage-gated sodium channels enable the translocation of sodium ions across cell membranes and play crucial roles in electrical signaling by initiating the action potential. In humans, mutations in sodium channels give rise to several neurological and cardiovascular diseases, and hence they are targets for pharmaceutical drug developments. Prokaryotic sodium channel crystal structures have pro...

Voltage-gated sodium channels (VGSCs) consist of a pore-forming α-subunit and regulatory β-subunits. Several families of neuroactive peptides of Conus snails target VGSCs, including μO-conotoxins and μ-conotoxins. Unlike μ-conotoxins and the guanidinium alkaloid saxitoxin (STX), which are pore blockers, μO-conotoxins MrVIA and MrVIB inhibit VGSCs by modifying channel gating. μO-MrVIA/B can bloc...