title: Glial reactions and degeneration of myelinated processes in spinal cord gray matter in chronic experimental autoimmune encephalomyelitis.
abstract: Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) result in inflammatory white matter lesions in the CNS. However, information is sparse with regard to the effects of autoimmune demyelinating disease on gray matter regions. Therefore, we studied the late effects of chronic EAE in C57BL/6 mice on the spinal cord gray matter using immunohistochemistry. Here, EAE induced marked astrocytic, microglial, and macrophage activation in the ventral horn gray matter, without any motoneuron loss. Activated caspase-3 was also increased in the ventral horn gray matter. Furthermore, activated poly (ADP-ribose) polymerase (PARP), another apoptotic marker, co-localized with myelin basic protein (MBP) of oligodendrocyte processes, but not with the oligodendroglial cell body marker, adenomatous polyposis coli gene clone CC1 (APC-CC1), or with neurofilament marker (RT-97) or synaptophysin of axonal arbors. However, there was no associated increase in the number of terminal deoxynucleotidyl transferase (TdT) mediated-dUTP nick end labeling positive nuclei in the spinal cord gray matter of EAE mice. In addition, co-localization of MBP and the low-affinity neurotrophin receptor, p75, was demonstrated, further supporting the notion of apoptotic oligodendrocyte process degeneration in the gray matter of EAE mice.
authors: Department of Neurology, David Geffen School of Medicine at University of California, Los Angeles, Charles Young Drive South, Los Angeles, CA 90095, USA.
authors: J
authors: J
authors: Wu
authors: M
authors: M
authors: Ohlsson
authors: E A
authors: EA
authors: Warner
authors: K K
authors: KK
authors: Loo
authors: T X
authors: TX
authors: Hoang
authors: R R
authors: RR
authors: Voskuhl
authors: L A
authors: LA
authors: Havton
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000870:Anterior Horn Cells / Q000378:metabolism / Q000473:pathology*; D015703:Antigens, CD / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000378:metabolism / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D020287:In Situ Nick-End Labeling / Q000379:methods; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D004676:Myelin Basic Protein / Q000378:metabolism; D009186:Myelin Sheath / Q000473:pathology*; D016900:Neurofilament Proteins / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D020800:Receptor, Nerve Growth Factor / Q000378:metabolism; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology*; D016708:Synaptophysin / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D005904:Glial Fibrillary Acidic Protein; D004676:Myelin Basic Protein; D016900:Neurofilament Proteins; D020800:Receptor, Nerve Growth Factor; D016708:Synaptophysin; C499321:Parp1 protein, mouse; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases; D053148:Caspase 3