title: Hippocampal Nogo-A and neo-Timm's staining in amygdala kindling rats.
abstract: OBJECTIVE
  Nogo-A, one of the axon regeneration inhibitors, has been shown to be up-regulated in both the experimental and human temporal lobe epilepsy. However, the role of Nogo-A in mossy fiber sprouting (MFS) relative to epileptogenesis is unknown. This work was designed to examine the relationship of the hippocampal Nogo-A protein expression with MFS during the development of amygdala kindling.
  
  
  METHODS
  Using immunohistochemistry and neo-Timm's histological procedures, we evaluated the distribution and density of Nogo-A and Nogo-66 receptor (Ng-R) expression and MFS in the bilateral hippocampus of amygdala kindling rats.
  
  
  RESULTS
  Nogo-A expression in the ipsilateral hippocampus gradually increased with the development of kindling in the sector CA2-3. In contrast, no increased Nogo-A expression was observed in the contralateral hippocampus as the rats advanced to stage 5 kindled seizures. Furthermore, poorer Nogo-A and Nogo-66 receptor (Ng-R) expression were observed in the dentate granule cells as aberrant MFS occurred.
  
  
  CONCLUSIONS
  In amygdala kindling rats, generalized stage 5 seizures were not associated with increased Nogo-A expression in the contralateral hippocampus supporting the concept that seizures by themselves do not induce Nogo-A expression. Furthermore, in the ipsilateral hippocampus, the expression of Nogo-A relative to MSF suggests that this protein may partially control aberrant synaptic reorganization during epileptogenesis.
authors: Department of Neurosurgery, Oita University Faculty of Medicine, Oita, Japan.
authors: Yu
authors: Y
authors: Takeda
authors: Tohru
authors: T
authors: Kamida
authors: Minoru
authors: M
authors: Fujiki
authors: Hidenori
authors: H
authors: Kobayashi
mesh_terms: D000679:Amygdala / Q000502:physiology; D000818:Animals; D004558:Electric Stimulation / Q000009:adverse effects; D004833:Epilepsy, Temporal Lobe / Q000378:metabolism* / Q000503:physiopathology; D007839:Functional Laterality / Q000502:physiology; D058851:GPI-Linked Proteins; D020439:Growth Cones / Q000378:metabolism / Q000473:pathology; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D007696:Kindling, Neurologic / Q000378:metabolism*; D008297:Male; D019599:Mossy Fibers, Hippocampal / Q000378:metabolism* / Q000473:pathology; D009185:Myelin Proteins / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology*; D000070798:Nogo Proteins; D000070816:Nogo Receptor 1; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000378:metabolism; D013194:Staining and Labeling / Q000379:methods; D015854:Up-Regulation / Q000502:physiology
chemical_list: D058851:GPI-Linked Proteins; D009185:Myelin Proteins; D000070798:Nogo Proteins; D000070816:Nogo Receptor 1; C000603199:RTN4 protein, human; D011956:Receptors, Cell Surface; C000603197:Rtn4 protein, rat; C486581:Rtn4r protein, rat