title: The temporal profile of the reaction of microglia, astrocytes, and macrophages in the delayed onset paraplegia after transient spinal cord ischemia in rabbits.
abstract: In the present study, we sought to elucidate the temporal profile of the reaction of microglia, astrocytes, and macrophages in the progression of delayed onset motor dysfunction after spinal cord ischemia (15 min) in rabbits. At 2, 4, 8, 12, 24, and 48 h after reperfusion (9 animals in each), hind limb motor function was assessed, and the lumbar spinal cord was histologically examined. Delayed motor dysfunction was observed in most animals at 48 h after ischemia, which could be predicted by a poor recovery of segmental spinal cord evoked potentials at 15 min of reperfusion. In the gray matter of the lumbar spinal cord, both microglia and astrocytes were activated early (2 h) after reperfusion. Microglia were diffusely activated and engulfed motor neurons irrespective of the recovery of segmental spinal cord evoked potentials. In contrast, early astrocytic activation was confined to the area where neurons started to show degeneration. Macrophages were first detected at 8 h after reperfusion and mainly surrounded the infarction area later. Although the precise roles of the activation of microglia, astrocytes, and macrophages are to be further determined, the results indicate that understanding functional changes of astrocytes may be important in the mechanism of delayed onset motor dysfunction including paraplegia.
  
  
  CONCLUSIONS
  Microglia and macrophages play a role in removing tissue debris after transient spinal cord ischemia. Disturbance of astrocytic defense mechanism, breakdown of the blood-spinal cord barrier, or both seemed to be involved in the development of delayed motor dysfunction.
authors.affiliation: Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsumoto
authors.forename: Mishiya
authors.initials: M
authors.lastname: Matsumoto
authors.forename: Atsuo
authors.initials: A
authors.lastname: Yamashita
authors.forename: Kazunobu
authors.initials: K
authors.lastname: Ohtake
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Ishida
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Morimoto
authors.forename: Takefumi
authors.initials: T
authors.lastname: Sakabe
mesh_terms: D000758:Anesthesia; D000818:Animals; D001253:Astrocytes / Q000473:pathology*; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001831:Body Temperature / Q000502:physiology; D018450:Disease Progression; D005071:Evoked Potentials / Q000187:drug effects; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006400:Hematocrit; D007150:Immunohistochemistry; D008262:Macrophage Activation / Q000502:physiology; D008264:Macrophages / Q000473:pathology*; D017628:Microglia / Q000473:pathology*; D009046:Motor Neurons / Q000473:pathology; D010264:Paraplegia / Q000473:pathology*; D011817:Rabbits; D015427:Reperfusion Injury / Q000473:pathology; D020760:Spinal Cord Ischemia / Q000473:pathology*; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D005904:Glial Fibrillary Acidic Protein