Action potential propagation in<unk> ated neurons is faster than in unmyelinated neurons because of Saltatory conduction. The main purpose of<unk>  is to increase the speed at which electrical impulses propagate along the<unk> ated fiber. In unmyelinated fibers, electrical impulses (action potentials) travel as continuous waves, but, in<unk> ated fibers, they "hop" or propagate by saltatory conduction. The latter is markedly faster than the former, at least for axons over a certain diameter.<unk>  decreases capacitance and increases electrical resistance across the axonal membrane (the axolemma). It has been suggested that<unk>  permits larger body size by maintaining agile communication between distant body parts.<unk> ated fibers lack voltage-gated sodium channels along the<unk> ated internodes, exposing them only at the nodes of Ranvier. Here, they are highly abundant and densely packed. Positively charged sodium ions can enter the axon through these voltage-gated channels, leading to depolarisation of the membrane potential at the node of Ranvier. The resting membrane potential is then rapidly restored due to positively charged potassium ions leaving the axon through potassium channels. The sodium ions inside the axon then diffuse rapidly through the axoplasm (axonal cytoplasm), to the adjacent<unk> ated internode and ultimately to the next (distal) node of Ranvier, triggering the opening of the voltage gated sodium channels and entry of sodium ions at this site. Although the sodium ions diffuse through the axoplasm rapidly, diffusion is decremental by nature, thus nodes of Ranvier have to be (relatively) closely spaced, to secure action potential propagation. The action potential "recharges" at consecutive nodes of Ranvier as the axolemmal membrane potential depolarises to approximately +35 mV. Along the<unk> ated internode, energy-dependent sodium/potassium pumps pump the sodium ions back out of the axon and potassium ions back into the axon to restore the balance of ions between the intracellular (inside the cell, i.e. axon in this case) and extracellular (outwith the cell) fluids. Whilst the role of<unk>  as an "axonal insulator" is well-established, other functions of<unk> ating cells are less well known or only recently established. The<unk> ating cell "sculpts" the underlying axon by promoting the phosphorylation of neurofilaments, thus increasing the diameter or thickness of the axon at the internodal regions; helps cluster molecules on the axolemma (such as voltage-gated sodium channels) at the node of Ranvier; and modulates the transport of cytoskeletal structures and organelles such as mitochondria, along the axon. In 2012, evidence came to light to support a role for the<unk> ating cell in "feeding" the axon. In other words, the<unk> ating cell seems to act as a local "fueling station" for the axon, which uses a great deal of energy to restore the normal balance of ions between it and its environment, following the generation of action potentials. When a peripheral fiber is severed, the<unk>  sheath provides a track along which regrowth can occur. However, the<unk>  layer does not ensure a perfect regeneration of the nerve fiber. Some regenerated nerve fibers do not find the correct muscle fibers, and some damaged motor neurons of the peripheral nervous system die without regrowth. Damage to the<unk>  sheath and nerve fiber is often associated with increased functional insufficiency. Unmyelinated fibers and<unk> ated axons of the mammalian central nervous system do not regenerate.
Myelin
Myelomere
Eribulin
Suramin
Zonulin
Mammaglobin
Fasciculin
Apamin