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Major histocompatibility complex class I expression and glial reaction influence spinal motoneuron synaptic plasticity during the course of experimental autoimmune encephalomyelitis.
J Comp Neurol. 2010 Apr 01; 518(7):990-1007.JC

Abstract

Recent studies have shown that major histocompatibility complex class I (MHC I) expression directly influences the stability of nerve terminals. Also, the acute phase of experimental autoimmune encephalomyelitis (EAE) has shown a significant impact on inputs within the spinal cord. Therefore, the present work investigated the synaptic covering of motoneurons during the induction phase of disease and progressive remissions of EAE. EAE was induced in C57BL/6J mice, which were divided into four groups: normal, peak disease, first remission, and second remission. The animals were killed and their lumbar spinal cords processed for in situ hybridization (IH), immunohistochemistry, and transmission electron microscopy (TEM). The results indicated an increase in glial reaction during the peak disease. During this period, the TEM analysis showed a reduction in the synaptic covering of the motoneurons, corresponding to a reduction in synaptophysin immunolabeling and an increase in the MHC I expression. The IH analysis reinforced the immunolabeling results, revealing an increased expression of MHC I mRNA by motoneurons and nonneuronal cells during the peak disease and first remission. The results observed in both remission groups indicated a return of the terminals to make contact with the motoneuron surface. The ratio between excitatory and inhibitory inputs increased, indicating the potential for development of an excitotoxic process. In conclusion, the results presented here indicate that MHC I up-regulation during the course of EAE correlates with the periods of synaptic plasticity induced by the infiltration of autoreactive immune cells and that synaptic plasticity decreases after recurrent peaks of inflammation.

Authors+Show Affiliations

Laboratory of Nerve Regeneration, Department of Anatomy, Institute of Biology, University of Campinas-UNICAMP, CEP 13083-970, Campinas, SP, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20127802

Citation

Freria, C M., et al. "Major Histocompatibility Complex Class I Expression and Glial Reaction Influence Spinal Motoneuron Synaptic Plasticity During the Course of Experimental Autoimmune Encephalomyelitis." The Journal of Comparative Neurology, vol. 518, no. 7, 2010, pp. 990-1007.
Freria CM, Zanon RG, Santos LM, et al. Major histocompatibility complex class I expression and glial reaction influence spinal motoneuron synaptic plasticity during the course of experimental autoimmune encephalomyelitis. J Comp Neurol. 2010;518(7):990-1007.
Freria, C. M., Zanon, R. G., Santos, L. M., & Oliveira, A. L. (2010). Major histocompatibility complex class I expression and glial reaction influence spinal motoneuron synaptic plasticity during the course of experimental autoimmune encephalomyelitis. The Journal of Comparative Neurology, 518(7), 990-1007. https://doi.org/10.1002/cne.22259
Freria CM, et al. Major Histocompatibility Complex Class I Expression and Glial Reaction Influence Spinal Motoneuron Synaptic Plasticity During the Course of Experimental Autoimmune Encephalomyelitis. J Comp Neurol. 2010 Apr 1;518(7):990-1007. PubMed PMID: 20127802.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Major histocompatibility complex class I expression and glial reaction influence spinal motoneuron synaptic plasticity during the course of experimental autoimmune encephalomyelitis. AU - Freria,C M, AU - Zanon,R G, AU - Santos,L M B, AU - Oliveira,A L R, PY - 2010/2/4/entrez PY - 2010/2/4/pubmed PY - 2010/5/6/medline SP - 990 EP - 1007 JF - The Journal of comparative neurology JO - J. Comp. Neurol. VL - 518 IS - 7 N2 - Recent studies have shown that major histocompatibility complex class I (MHC I) expression directly influences the stability of nerve terminals. Also, the acute phase of experimental autoimmune encephalomyelitis (EAE) has shown a significant impact on inputs within the spinal cord. Therefore, the present work investigated the synaptic covering of motoneurons during the induction phase of disease and progressive remissions of EAE. EAE was induced in C57BL/6J mice, which were divided into four groups: normal, peak disease, first remission, and second remission. The animals were killed and their lumbar spinal cords processed for in situ hybridization (IH), immunohistochemistry, and transmission electron microscopy (TEM). The results indicated an increase in glial reaction during the peak disease. During this period, the TEM analysis showed a reduction in the synaptic covering of the motoneurons, corresponding to a reduction in synaptophysin immunolabeling and an increase in the MHC I expression. The IH analysis reinforced the immunolabeling results, revealing an increased expression of MHC I mRNA by motoneurons and nonneuronal cells during the peak disease and first remission. The results observed in both remission groups indicated a return of the terminals to make contact with the motoneuron surface. The ratio between excitatory and inhibitory inputs increased, indicating the potential for development of an excitotoxic process. In conclusion, the results presented here indicate that MHC I up-regulation during the course of EAE correlates with the periods of synaptic plasticity induced by the infiltration of autoreactive immune cells and that synaptic plasticity decreases after recurrent peaks of inflammation. SN - 1096-9861 UR - https://www.unboundmedicine.com/medline/citation/20127802/Major_histocompatibility_complex_class_I_expression_and_glial_reaction_influence_spinal_motoneuron_synaptic_plasticity_during_the_course_of_experimental_autoimmune_encephalomyelitis_ L2 - https://doi.org/10.1002/cne.22259 DB - PRIME DP - Unbound Medicine ER -