The response of oligodendrocytes to chemical injury.
Oligodendrocytes establish relationships with axons at myelination which commit the cell to make and then maintain certain volumes of myelin. As a result of this oligodendrocytes are a heterogenous population of cells. At one extreme, large cells support a single internode on large diameter axons while at the other, small cells support many internodes on small diameter axons. Although it is common practice to separate chemicals which cause vacuolation of myelin sheaths from those which bring about cell death and thus demyelination, many compounds produce vacuolation and/or cell degeneration depending on concentration; an observation which suggests that myelin sheath-associated vacuolation reflects oligodendrocyte toxicity rather than a specific myelinopathy. The restoration of myelin sheath-axon relationships following chemically induced demyelination requires a complex sequence of cell-cell interactions to occur in an orderly manner if new myelin sheaths are to be formed. Recruitment of new oligodendrocytes can be separated from the interaction of oligodendrocytes with axons which results in the laying down of a myelin sheath. The latter event can only take place in the absence of demyelinating agents and in the presence of astrocytes.
D015120:6-Aminonicotinamide / Q000633:toxicity; D000818:Animals; D001369:Axons / Q000648:ultrastructure; D003471:Cuprizone / Q000633:toxicity; D003711:Demyelinating Diseases / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D004996:Ethidium / Q000633:toxicity; D007538:Isoniazid / Q000633:toxicity; D051379:Mice; D009186:Myelin Sheath / Q000502:physiology; D009457:Neuroglia / Q000187:drug effects*; D009836:Oligodendroglia / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D051381:Rats; D014267:Triethyltin Compounds / Q000633:toxicity
D014267:Triethyltin Compounds; D015120:6-Aminonicotinamide; D003471:Cuprizone; C031575:triethyltin; D004996:Ethidium; D007538:Isoniazid