The elucidation of depression and treatment-resistant depression for interaction of neuron and astrocyte function

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590657
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Applied pharmacology
• Research Institution: Okayama University
• Principal Investigator: KITAMURA YOSHIHISA 岡山大学, 大学病院, 准教授 (40423339)
• Co-Investigator(Kenkyū-buntansha): ASANUMA Masato 岡山大学, 大学院医歯薬学総合研究科, 教授 (00273970)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 治療抵抗性うつ病 / 神経新生 / 電気けいれん療法 / セロトニン1A受容体 / 脳由来神経栄養因子

Outline of Final Research Achievements

We previously reported that chronic treatment of rats with ACTH may be an effective model of tricyclic antidepressant treatment-resistant conditions. Electroconvulsive stimuli and 8-OH-DPAT increased cell proliferation in both saline-treated and ACTH-treated rats. Electroconvulsive stimuli and 5-HT1A receptor full agonist, 8-OH-DPAT significantly decreased the duration of immobility following repeated administration of ACTH. Electroconvulsive stimuli treatment increased mature-brain-derived neurotrophic factor (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 and 5-HT1A receptor full agonist may be attributed, at least in part, to an enhancement of hippocampal cell proliferation.

Free Research Field

精神神経薬理学