کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4181326 1276654 2006 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Corticosterone-Induced Inhibition of Gliogenesis in Rat Hippocampus is Counteracted by Electroconvulsive Seizures
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی روانپزشکی بیولوژیکی
پیش نمایش صفحه اول مقاله
Corticosterone-Induced Inhibition of Gliogenesis in Rat Hippocampus is Counteracted by Electroconvulsive Seizures
چکیده انگلیسی

BackgroundVolumetric 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.MethodsRats 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.ResultsECS 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.ConclusionsOur 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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biological Psychiatry - Volume 59, Issue 2, 15 January 2006, Pages 178–186
نویسندگان
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