The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats
The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats
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DOI：
10.1254/jphs.13015fp
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发表时间：
2013-05-01
影响因子：
3.5
通讯作者：
Sendo, Toshiaki
中科院分区：
文献类型：
--
作者：
Kuwatsuka, Keiko;Hayashi, Hiromi;Sendo, Toshiaki
在临床研究中，电惊厥刺激与抑郁症和难治性抑郁症的改善有关。在先前的研究中，用促肾上腺皮质激素（ACTH）治疗14天可降低成年海马细胞增殖。此外，电惊厥刺激显着减少了不动的持续时间后，反复给药促肾上腺皮质激素为14天的大鼠。本研究通过测定ACTH处理大鼠海马中细胞增殖、脑源性神经营养因子（BDNF）水平、磷酸化和总环磷酸腺苷（cAMP）反应元件结合蛋白（pCREB/CREB）水平，进一步表征电惊厥刺激的治疗抵抗性抗抑郁作用的机制。电惊厥刺激增加细胞增殖在盐水治疗和ACTH治疗的大鼠。成熟的BDNF蛋白水平表现出下降的趋势，在ACTH治疗的大鼠。电惊厥刺激治疗增加了成熟的BDNF蛋白水平在海马的生理盐水处理和ACTH处理的大鼠。此外，电惊厥刺激增加磷酸丝氨酸133-CREB（pCREB）水平和比例的pCREB/CREB在生理盐水处理和ACTH处理的大鼠。这些结果表明，治疗耐药的抗抑郁作用的电惊厥刺激可能是由于，至少部分，海马细胞增殖的增强。
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.