title: Neuronal damage and plasticity identified by microtubule-associated protein 2, growth-associated protein 43, and cyclin D1 immunoreactivity after focal cerebral ischemia in rats.
abstract: OBJECTIVE
  An objective of therapeutic intervention after cerebral ischemia is to promote improved functional outcome. Improved outcome may be associated with a reduction of the volume of cerebral infarction and the promotion of cerebral plasticity. In the developing brain, neuronal growth is concomitant with expression of particular proteins, including microtubule-associated protein 2 (MAP-2), growth-associated protein 43 (GAP-43), and cyclin D1. In the present study we measured the expression of select proteins associated with neurite damage and plasticity (MAP-2 and GAP-43) as well as cell cycle (cyclin D1) after induction of focal cerebral ischemia in the rat.
  
  
  METHODS
  Brains from rats (n=28) subjected to 2 hours of middle cerebral artery occlusion and 6 hours, 12 hours, and 2, 7, 14, 21, and 28 days (n=4 per time point) of reperfusion and control sham-operated (n=3) and normal (n=2) rats were processed by immunohistochemistry with antibodies raised against MAP-2, GAP-43, and cyclin D1. Double staining of these proteins for cellular colocalization was also performed.
  
  
  RESULTS
  Loss of immunoreactivity of both MAP-2 and GAP-43 was observed in most damaged neurons in the ischemic core. In contrast, MAP-2, GAP-43, and cyclin D1 were selectively increased in morphologically intact or altered neurons localized to the ischemic core at an early stage (eg, 6 hours) of reperfusion and in the boundary zone to the ischemic core (penumbra) during longer reperfusion times.
  
  
  CONCLUSIONS
  The selective expressions of the neuronal structural proteins (MAP-2 in dendrites and GAP-43 in axons) and the cyclin D1 cell cycle protein in neurons observed in the boundary zone to the ischemic core are suggestive of compensatory and repair mechanisms in ischemia-damaged neurons after transient focal cerebral ischemia.
authors.affiliation: Department of Neurology, Henry Ford Health Sciences Center, Detroit, Mich, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: N
authors.initials: N
authors.lastname: Jiang
authors.forename: C
authors.initials: C
authors.lastname: Powers
authors.forename: M
authors.initials: M
authors.lastname: Chopp
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000378:metabolism; D001923:Brain Chemistry; D019938:Cyclin D1 / Q000032:analysis* / Q000276:immunology; D019922:GAP-43 Protein / Q000032:analysis* / Q000276:immunology; D007124:Immunoenzyme Techniques; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000032:analysis* / Q000276:immunology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000737:chemistry / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D019922:GAP-43 Protein; D008869:Microtubule-Associated Proteins; D019938:Cyclin D1