Cloning, distribution and functional analysis of the type III sodium channel from human brain

The type III voltage-gated sodium channel was cloned from human brain. The full-length cDNA has 89% identity with rat type III, and the predicted protein (1951 amino acids) has 55 differences. The expression pattern of human type III mRNA was determined in adult brain tissue and, in contrast to rat, was detected in many regions, including caudate nucleus, cerebellum, hippocampus and frontal lobe. The human type III channel was stably expressed in Chinese hamster ovary (CHO) cells and its biophysical properties compared to the human type II channel using identical conditions. The voltage dependence and kinetics of activation were found to be similar to that of type II. The kinetics of inactivation of the two human subtypes were also similar. However, type III channels inactivated at more hyperpolarized potentials and were slower to recover from inactivation than type II. When expressed in human embryonic kidney (HEK293T) cells, type III channels produced currents with a prominent persistent component, which were similar to those reported for rat type II [Ma et al. (1997) Neuron, 19, 443-452]. However, unlike type II, this was prominent even in the absence of coexpressed G-proteins, suggesting type III may adopt this gating mode more readily. The distinct properties of the channel, together with its wide distribution in adult brain, suggest that in humans, type III may have important physiological roles under normal, and perhaps also pathological conditions.     

Effects of occlusal forces on the peri‐implant‐bone interface stability

The occlusal forces and their influence on the initiation of peri‐implant bone loss or their relationship with peri‐implantitis have created discussion during the past 30 years given the discrepancies observed in clinical, animal, and finite element analysis studies. Beyond these contradictions, in the case of an osseointegrated implant, the occlusal forces can influence the implant‐bone interface and the cells responsible for the bone remodeling in different ways that may result in the maintenance or loss of the osseointegration. This comprehensive review focuses on the information available about the forces transmitted through the implant‐crown system to the implant‐bone interface and the mechano‐transduction phenomena responsible for the bone cells’ behavior and their interactions. Knowledge of the basic molecular biology of the peri‐implant bone would help clinicians to understand the complex phenomenon of occlusal forces and their effects on the implant‐bone interface, and would allow better control of the negative effects of mechanical stresses, leading to therapy with fewer risks and complications.