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Volume 59, Issue 2, Pages 178-186 (15 January 2006)


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Corticosterone-Induced Inhibition of Gliogenesis in Rat Hippocampus is Counteracted by Electroconvulsive Seizures

Malin Wennström, Johan Hellsten, Joakim Ekstrand, Hanna Lindgren, Anders TingströmCorresponding Author Informationemail address

Received 17 March 2005; received in revised form 8 July 2005; accepted 16 August 2005.

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-100β 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.

Molecular Psychiatry Unit, Wallenberg Neuroscience Center, Lund, Sweden

Corresponding Author InformationAddress reprint requests to Anders Tingström, M.D., Ph.D., Molecular Psychiatry Unit, Wallenberg Neuroscience Center, BMC A13, S-22184, Lund, Sweden

PII: S0006-3223(05)01327-2

doi:10.1016/j.biopsych.2005.08.032


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