Nodes of Ranvier (/ˈrɑːnvieɪ/ RAHN-vee-ay),[1][2] also known as myelin-sheath gaps, occur along a myelinated axon where the axolemma is exposed to the extracellular space.

The nodes are primarily composed of sodium and potassium voltage-gated ion channels; CAMs such as neurofascin-186 and NrCAM; and cytoskeletal adaptor proteins such as ankyrin-G and spectrinβIV.

[4] Many vertebrate axons are surrounded by a myelin sheath, allowing rapid and efficient saltatory ("jumping") propagation of action potentials.

This organization demands a tight developmental control and the formation of a variety of specialized zones of contact between different areas of the myelinating cell membrane.

Each node of Ranvier is flanked by paranodal regions where helicoidally wrapped glial loops are attached to the axonal membrane by a septate-like junction.

The segment between nodes of Ranvier is termed as the internode, and its outermost part that is in contact with paranodes is referred to as the juxtaparanodal region.

The nodes are encapsulated by microvilli stemming from the outer aspect of the Schwann cell membrane in the PNS, or by perinodal extensions from astrocytes in the CNS.

The size and the spacing of the internodes vary with the fiber diameter in a curvilinear relationship that is optimized for maximal conduction velocity.

[5] The size of the nodes span from 1–2 μm whereas the internodes can be up to (and occasionally even greater than)1.5 millimetres long, depending on the axon diameter and fiber type.

The structure of the node and the flanking paranodal regions are distinct from the internodes under the compact myelin sheath, but are very similar in CNS and PNS.

The decreased axon size reflects a higher packing density of neurofilaments in this region, which are less heavily phosphorylated and are transported more slowly.

[6] Vesicles and other organelles are also increased at the nodes, which suggest that there is a bottleneck of axonal transport in both directions as well as local axonal-glial signaling.

Although freeze fracture studies have revealed that the nodal axolemma in both the CNS and PNS is enriched in intra-membranous particles (IMPs) compared to the internode, there are some structural differences reflecting their cellular constituents.

[6] In the PNS, specialized microvilli project from the outer collar of Schwann cells and come very close to nodal axolemma of large fibers.

At CNS nodes, the axonal proteins also include contactin; however, different from the PNS, Schwann cell microvilli are replaced by astrocyte perinodal extensions.

In the CNS, oligodendrocytes do not possess microvilli, but appear capable to initiate the clustering of some axonal proteins through secreted factors.

The combined effects of such factors with the subsequent movements generated by the wrapping of oligodendrocyte periaxonal extension could account for the organization of CNS nodes of Ranvier.

[17] The actual physiological role of this accumulation and factors that regulate it are not understood; however, it is known that mitochondria are usually present in areas of the cell that expresses a high energy demand.

In these same regions, they are also understood to contain growth cones, synaptic terminals, and sites of action potential initiation and regeneration, such as the nodes of Ranvier.

In the nodes of Ranvier, mitochondria serve as an important role in impulse conduction by producing the ATP that is essential to maintain the activity of energy-demanding ion pumps.

Supporting this fact, about five times more mitochondria are present in the PNP axoplasm of large peripheral axons than in the corresponding internodal regions of these fibers.

[17] Saltatory conduction in myelinated axons requires organization of the nodes of Ranvier, whereas voltage-gated sodium channels are highly populated.

[18] It is also proven that αII-Spectrin in the axonal cytoskeleton is absolutely vital for stabilizing sodium channel clusters and organizing the mature node of Ranvier.

[22] French pathologist and anatomist Louis-Antoine Ranvier later discovered the nodes, or gaps, in the myelin sheath that now bear his name.