Disease relevance of Ranvier's Nodes

• Light microscopic, and scanning and transmission electron microscopic studies of the nodes of Ranvier of the distal peripheral nerves of mice with muscular dystrophy (dy/dy) are reported [1].
• Immunohistochemical study data demonstrated that transplanted BMSCs labeled with retrovirus green fluorescent protein were positive for P0 and myelin-associated glycoprotein and had reconstructed nodes of Ranvier and remyelinated regenerated nerve axons [2].
• We present evidence for morphological changes within 15 min of injury where aggregates of pyroantimonate precipitate occur in nodal blebs at nodes of Ranvier, in focal swellings within axonal mitochondria, and at localized sites of separation of myelin lamellae [3].

High impact information on Ranvier's Nodes

• We therefore now report a comparison of the effects of a vegetable toxin (oenanthotoxin or OETX) on both sodium current (INa) and intra-membrane charge movement (Q) in Ranvier nodes [4].
• Asymmetrical currents and sodium currents in Ranvier nodes exposed to DDT [5].
• We propose that gliomedin provides a glial cue for the formation of peripheral nodes of Ranvier [6].
• Dystroglycan may be required for the normal maintenance of voltage-gated sodium channels at nodes of Ranvier, possibly by mediating trans interactions between Schwann cell microvilli and the nodal axolemma [7].
• The contactin mutation does not affect sodium channel clustering at the nodes of Ranvier but alters the location of the Shaker-type Kv1.1 and Kv1.2 potassium channels [8].

Biological context of Ranvier's Nodes

• We report the identification of gliomedin, a glial ligand for neurofascin and NrCAM, two axonal immunoglobulin cell adhesion molecules that are associated with Na+ channels at the nodes of Ranvier [6].
• Administration to mice of a 0.1% solution of pyronin G in their drinking water caused an acceleration both of axonal sprouting from nodes of Ranvier in partly denervated gluteus maximus muscles, and of motor nerve regeneration following a crush to the soleus nerve [9].
• The lectin cytochemistry indicates that the 170 K Dalton glycoprotein with PNA affinity obtained from rat sciatic nerves occurs in nodes of Ranvier [10].
• In the optic nerve, the fastest components of the compound action potential are slowed and the number of mature nodes of Ranvier is reduced, but Na(v)1.6, contactin, caspr 1, and K(v)1 channels are all localized normally at nodes [11].

Anatomical context of Ranvier's Nodes

• When compaction of myelin occurred, MAG remained present only at the axon-Schwann cell interface; Schmidt-Lanterman incisures, inner and outer mesaxons, and paranodal loops, but not at finger-like processes of Schwann cells at nodes of Ranvier or compacted myelin [12].
• In skeletal muscle, amphiphysin II is concentrated around T tubules, while in brain it is concentrated in the cytomatrix beneath the plasmamembrane of axon initial segments and nodes of Ranvier [13].
• In the experimental model, antibody is concentrated in specialized myelin structures, the nodes of Ranvier, and Schmidt-Lanterman incisures, suggesting that myelin-associated glycoprotein may be the antigenic target in vivo [14].
• Our results reveal a previously unknown role for nsf, independent of its function in synaptic vesicle fusion, in the formation of the nodes of Ranvier in the vertebrate nervous system [15].
• However, cytotactin was concentrated at the neuromuscular junctions as well as at the nodes of Ranvier [16].

Associations of Ranvier's Nodes with chemical compounds

• Motor axons in formamide-treated inactive muscle sprouted only from their terminal arborizations, but not from nodes of Ranvier [17].
• Identification of O-linked N-acetylglucosamine modification of ankyrinG isoforms targeted to nodes of Ranvier [18].
• It is suggested that the increase in threshold produced by sevoflurane is due to depression of Na(+) currents at the nodes of Ranvier of corticospinal axons [19].
• Antibodies against the serine-rich domain and spectrin-binding domain revealed labeling of nodes of Ranvier and axonal initial segments [20].
• No segmental demyelination or remyelination was found, but the nodes of Ranvier were slightly widened and paronodal bulbi were swollen relative to fibre calibre [21].

Gene context of Ranvier's Nodes

• Early onset of degenerative changes at nodes of Ranvier in alpha-motor axons of Cntf null (-/-) mutant mice [22].
• We show here that KCNQ2 channels are functional components of axon initial segments and nodes of Ranvier, colocalizing with ankyrin-G and voltage-dependent Na+ channels throughout the CNS and PNS [23].
• NrCAM, visualized with antibodies specific for the ecto-domain, also was found to be coexpressed with neurofascin at nodes of Ranvier and at axon initial segments [24].
• Both laminin and Schwann cell dystroglycan are necessary for proper clustering of sodium channels at nodes of Ranvier [25].
• [Beta]IV-spectrin regulates sodium channel clustering through ankyrin-G at axon initial segments and nodes of Ranvier [26].

Analytical, diagnostic and therapeutic context of Ranvier's Nodes

• 8. Immunohistochemistry localized the glycoprotein at the nodes of Ranvier and at the periphery of neurons [27].
• The elongated nerves also showed paranodal demyelination in Ranvier's nodes longer than those in the control group [28].

References