title: Impact of pregabalin treatment on synaptic plasticity and glial reactivity during the course of experimental autoimmune encephalomyelitis.
abstract: BACKGROUND
  Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease that affects young adults. It is characterized by generating a chronic demyelinating autoimmune inflammation in the central nervous system. An experimental model for studying MS is the experimental autoimmune encephalomyelitis (EAE), induced by immunization with antigenic proteins from myelin.
  
  
  OBJECTIVE
  The present study investigated the evolution of EAE in pregabalin treated animals up to the remission phase.
  
  
  RESULTS
  The results demonstrated a delay in the onset of the disease with statistical differences at the 10th and the 16th day after immunization. Additionally, the walking track test (CatWalk) was used to evaluate different parameters related to motor function. Although no difference between groups was obtained for the foot print pressure, the regularity index was improved post treatment, indicating a better motor coordination. The immunohistochemical analysis of putative synapse preservation and glial reactivity revealed that pregabalin treatment improved the overall morphology of the spinal cord. A preservation of circuits was depicted and the glial reaction was downregulated during the course of the disease. qRT-PCR data did not show immunomodulatory effects of pregabalin, indicating that the positive effects were restricted to the CNS environment.
  
  
  CONCLUSIONS
  Overall, the present data indicate that pregabalin is efficient for reducing the seriousness of EAE, delaying its course as well as reducing synaptic loss and astroglial reaction.
authors.affiliation: Laboratory of Nerve Regeneration, Department of Structural and Functional Biology, Institute of Biology, University of Campinas - UNICAMP Campinas, SP, Brazil.
authors.forename: Gleidy A A
authors.initials: GA
authors.lastname: Silva
authors.affiliation: Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil ; Neuroimmunomodulation Group, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil.
authors.forename: Fernando
authors.initials: F
authors.lastname: Pradella
authors.affiliation: Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil ; Neuroimmunomodulation Group, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil.
authors.forename: Adriel
authors.initials: A
authors.lastname: Moraes
authors.affiliation: Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil ; Neuroimmunomodulation Group, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Farias
authors.affiliation: Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas - UNICAMP Campinas, SP, Brazil.
authors.forename: Leonilda M B
authors.initials: LM
authors.lastname: dos Santos
authors.affiliation: Laboratory of Nerve Regeneration, Department of Structural and Functional Biology, Institute of Biology, University of Campinas - UNICAMP Campinas, SP, Brazil.
authors.forename: Alexandre L R
authors.initials: AL
authors.lastname: de Oliveira
mesh_terms: D000818:Animals; D002135:Calcium-Binding Proteins / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000188:drug therapy / Q000503:physiopathology; D007150:Immunohistochemistry; D008840:Microfilament Proteins / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009046:Motor Neurons / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D009457:Neuroglia / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D000069583:Pregabalin; D011917:Rats, Inbred Lew; D060888:Real-Time Polymerase Chain Reaction; D013116:Spinal Cord / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D013569:Synapses / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D016708:Synaptophysin / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: C100745:Aif1 protein, rat; D002135:Calcium-Binding Proteins; D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D008840:Microfilament Proteins; D018696:Neuroprotective Agents; D016708:Synaptophysin; C569016:Syp protein, rat; D000069583:Pregabalin; D005680:gamma-Aminobutyric Acid
keywords: Experimental autoimmune encephalomyelitis; pregabalin; spinal motoneurons; synapse