title: The mechanisms of electroconvulsive stimuli in BrdU-positive cells of the dentate gyrus in ACTH-treated rats.
abstract: In clinical studies, electroconvulsive stimuli have been associated with improvements in both depression and treatment-resistant depression. In a previous study, treatment with adrenocorticotropic hormone (ACTH) for 14 days decreased adult hippocampal cell proliferation. Furthermore, electroconvulsive stimuli significantly decreased the duration of immobility following repeated administration of ACTH for 14 days in rats. The present study was undertaken to further characterize the mechanism of treatmentresistant antidepressant effects of electroconvulsive stimuli by measuring cell proliferation, brain-derived neurotrophic factor (BDNF) levels, and phosphorylated and total cyclic adenosine monophosphate (cAMP) response element-binding protein (pCREB/CREB) levels in the hippocampus of ACTH-treated rats. Electroconvulsive stimuli increased cell proliferation in both saline-treated and ACTH-treated rats. Mature-BDNF protein levels showed a tendency to decrease in ACTH-treated rats. Electroconvulsive stimuli treatment increased mature-BDNF protein levels in the hippocampus of both saline-treated and ACTH-treated rats. Furthermore, electroconvulsive stimuli increased phospho-Ser133-CREB (pCREB) levels and the ratio of pCREB/CREB in both saline-treated and ACTH-treated rats. These findings suggest that the treatment-resistant antidepressant effects of electroconvulsive stimuli may be attributed, at least in part, to an enhancement of hippocampal cell proliferation.
authors.affiliation: Department of Clinical Pharmacy, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Japan.
authors.forename: Keiko
authors.initials: K
authors.lastname: Kuwatsuka
authors.forename: Hiromi
authors.initials: H
authors.lastname: Hayashi
authors.forename: Yuka
authors.initials: Y
authors.lastname: Onoue
authors.forename: Ikuko
authors.initials: I
authors.lastname: Miyazaki
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Koyama
authors.forename: Masato
authors.initials: M
authors.lastname: Asanuma
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Kitamura
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Sendo
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D001973:Bromodeoxyuridine; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004565:Electroconvulsive Therapy; D006624:Hippocampus / Q000166:cytology* / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020800:Receptor, Nerve Growth Factor / Q000378:metabolism; D020813:Receptor, trkB / Q000378:metabolism
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D017362:Cyclic AMP Response Element-Binding Protein; D020800:Receptor, Nerve Growth Factor; D000324:Adrenocorticotropic Hormone; D020813:Receptor, trkB; D001973:Bromodeoxyuridine