Tumour necrosis factor causes an increase in axonal transport of protein and demyelination in the mouse optic nerve
Identifieur interne : 001366 ( Main/Curation ); précédent : 001365; suivant : 001367Tumour necrosis factor causes an increase in axonal transport of protein and demyelination in the mouse optic nerve
Auteurs : Huw G. Jenkins [Royaume-Uni] ; Hisako Ikeda [Royaume-Uni]Source :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1992.
English descriptors
- Teeft :
- Axonal, Axonal transport, Blood vessel, Colliculi, Colliculus, Demyelination, Electron micrograph, Ikeda, Intraocular injection, Intravitreal, Intravitreal injection, Intravitreal injections, Liquid scintillation, Mouse, Mouse vitreous, Multiple sclerosis, Myelin, Myelin destruction, Myelinated axons, Nude mice, Optic, Optic nerve, Optic nerve demyelination, Optic nerve fibres, Optic nerve section, Optic nerve sections, Optic nerves, Retina, Rtnf, Rtnf injection, Sclerosis, Semliki, Semliki forest virus, Semliki forest virus infection, Superior colliculi, Superior colliculus, Tansey, Units rtnf.
Abstract
Abstract: An increase in fast axonal transport of protein by the optic nerve was found in mice following a single combined injection of human recombinant tumour necrosis factor alpha (rTNF) and [3H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at lease some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.
Url:
DOI: 10.1016/0022-510X(92)90194-P
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<term>Colliculi</term>
<term>Colliculus</term>
<term>Demyelination</term>
<term>Electron micrograph</term>
<term>Ikeda</term>
<term>Intraocular injection</term>
<term>Intravitreal</term>
<term>Intravitreal injection</term>
<term>Intravitreal injections</term>
<term>Liquid scintillation</term>
<term>Mouse</term>
<term>Mouse vitreous</term>
<term>Multiple sclerosis</term>
<term>Myelin</term>
<term>Myelin destruction</term>
<term>Myelinated axons</term>
<term>Nude mice</term>
<term>Optic</term>
<term>Optic nerve</term>
<term>Optic nerve demyelination</term>
<term>Optic nerve fibres</term>
<term>Optic nerve section</term>
<term>Optic nerve sections</term>
<term>Optic nerves</term>
<term>Retina</term>
<term>Rtnf</term>
<term>Rtnf injection</term>
<term>Sclerosis</term>
<term>Semliki</term>
<term>Semliki forest virus</term>
<term>Semliki forest virus infection</term>
<term>Superior colliculi</term>
<term>Superior colliculus</term>
<term>Tansey</term>
<term>Units rtnf</term>
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<front><div type="abstract" xml:lang="en">Abstract: An increase in fast axonal transport of protein by the optic nerve was found in mice following a single combined injection of human recombinant tumour necrosis factor alpha (rTNF) and [3H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at lease some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.</div>
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