title: Corticosterone-induced inhibition of gliogenesis in rat hippocampus is counteracted by electroconvulsive seizures.
abstract: BACKGROUND
  Volumetric changes and glial pathology have been reported in the central nervous system (CNS) of patients with depressive disorder, an illness often associated with elevated glucocorticoid levels. Glucocorticoids reduce gliogenesis in the adult rat CNS. Electroconvulsive seizure (ECS)-treatment, an animal model for the antidepressant treatment electroconvulsive therapy, can enhance proliferation of glial cells. This study examined glial cell proliferation in response to ECS in rats whose glucocorticoid levels were elevated to mimic the conditions seen in depression.
  
  
  METHODS
  Rats were injected daily for seven days with either corticosterone or vehicle. ECS- or sham- treatment was given once daily during the first five days. Proliferating cells in the hippocampus were labeled with bromodeoxyuridine and analyzed for co-labeling with the glial cell markers NG2, Ox42, S-100beta and Rip.
  
  
  RESULTS
  ECS counteracted the glucocorticoid-induced inhibition of NG2+, Ox42+ and Rip+ cell proliferation, and the gliogenesis rate was restored to baseline levels. Volumetric changes in rats treated with ECS were detected.
  
  
  CONCLUSIONS
  Our results show that ECS-treatment affects the proliferation of glial cells even in the presence of elevated levels of glucocorticoids. This result adds to an increasing number of studies suggesting that antidepressant treatment can counteract degenerative processes associated with major depression.
authors.affiliation: Molecular Psychiatry Unit, Wallenberg Neuroscience Center, S-22184, Lund, Sweden.
authors.forename: Malin
authors.initials: M
authors.lastname: Wennström
authors.forename: Johan
authors.initials: J
authors.lastname: Hellsten
authors.forename: Joakim
authors.initials: J
authors.lastname: Ekstrand
authors.forename: Hanna
authors.initials: H
authors.lastname: Lindgren
authors.forename: Anders
authors.initials: A
authors.lastname: Tingström
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism; D002452:Cell Count; D002454:Cell Differentiation / Q000502:physiology*; D049109:Cell Proliferation; D003345:Corticosterone / Q000502:physiology*; D003863:Depression / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004597:Electroshock; D006624:Hippocampus / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D007150:Immunohistochemistry; D008297:Male; D009836:Oligodendroglia / Q000166:cytology / Q000502:physiology*; D009929:Organ Size; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000473:pathology* / Q000503:physiopathology; D013234:Stem Cells / Q000166:cytology / Q000502:physiology*; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D003345:Corticosterone; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4