The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats

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, electroconvulsi...

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Published in:Journal of Pharmacological Sciences 2013/05/20, Vol.122(1), pp.34-41
Main Authors: Kuwatsuka, Keiko, Hayashi, Hiromi, Onoue, Yuka, Miyazaki, Ikuko, Koyama, Toshihiro, Asanuma, Masato, Kitamura, Yoshihisa, Sendo, Toshiaki
Format: Article
Language:English
Subjects:
adrenocorticotropic hormone
Adrenocorticotropic Hormone - pharmacology
Animals
brain derived neurotrophic factor
Brain-Derived Neurotrophic Factor - metabolism
Bromodeoxyuridine
cAMP response element binding protein
cell proliferation
Cyclic AMP Response Element-Binding Protein - metabolism
electroconvulsive stimuli
Electroconvulsive Therapy
Hippocampus - cytology
Hippocampus - metabolism
Rats
Rats, Wistar
Receptor, Nerve Growth Factor - metabolism
Receptor, trkB - metabolism
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Summary: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 treatment-resistant 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.
ISSN:1347-8613
1347-8648
DOI:10.1254/jphs.13015FP