title: High-affinity NGF receptor in the rat spinal cord during acute and chronic phases of experimental autoimmune encephalomyelitis: a possible functional significance.
abstract: The biological effects of Nerve Growth Factor (NGF) are primarily mediated via its high affinity receptor-TrkA. In the present study, we examined the effect of experimental autoimmune encephalomyelitis (EAE) upon the expression of TrkA in neuronal and non-neuronal cells of the spinal cord of Lewis rats during the acute (14 days postimmunization) and chronic (12 months postimmunization) phases of the disease. In the normal spinal cord, both of mature and aged rats, we found TrkA immunoreaction (TrkA-IR) in the motoneurons of the Rexed lamina IX and in both oligo- and astroglia cells. In the acute phase of the disease, we found a reduction of TrkA immunoreactivity in motoneurons and its up-regulation in oligodendroglia, mainly in the white matter. We also confirmed our previous findings concerning the up-regulation of TrkA-IR in astroglia. Both neuronal and non-neuronal changes of TrkA immunoreactivity had a transient character: they were not seen in the chronic phase of the disease. Our results suggest that both neuronal and glial TrkA expression changes depend on inflammation. Moreover, our data indicate that, during the acute phase of EAE, the glial cells become more receptive to NGF, pointing to glia as an important target for pharmacological manipulations, particularly for exogenously administered NGF.
authors.affiliation: Nencki Institute of Experimental Biology, PAN, Polish Academy of Sciences, 02 093 Warsaw, Pasteura 3, Poland. oderfeld@nencki.gov.pl
authors.forename: B
authors.initials: B
authors.lastname: Oderfeld-Nowak
authors.forename: M
authors.initials: M
authors.lastname: Zaremba
authors.forename: A W
authors.initials: AW
authors.lastname: Lipkowski
authors.forename: B
authors.initials: B
authors.lastname: Kwiatkowska-Patzer
authors.forename: V
authors.initials: V
authors.lastname: Triaca
authors.forename: L
authors.initials: L
authors.lastname: Aloe
mesh_terms: D000208:Acute Disease; D000375:Aging / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004351:Drug Resistance / Q000502:physiology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D009046:Motor Neurons / Q000378:metabolism / Q000473:pathology; D009103:Multiple Sclerosis / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000473:pathology; D020932:Nerve Growth Factor / Q000378:metabolism* / Q000494:pharmacology; D009836:Oligodendroglia / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051381:Rats; D011917:Rats, Inbred Lew; D020917:Receptor, trkA / Q000378:metabolism*; D013116:Spinal Cord / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D020932:Nerve Growth Factor; D020917:Receptor, trkA