PMID- 25820756 OWN - NLM STAT- MEDLINE DCOM- 20160420 LR - 20181113 IS - 1573-6830 (Electronic) IS - 0272-4340 (Linking) VI - 35 IP - 6 DP - 2015 Aug TI - Time Course of Behavioral Alteration and mRNA Levels of Neurotrophic Factor Following Stress Exposure in Mouse. PG - 807-17 LID - 10.1007/s10571-015-0174-x [doi] AB - Stress is known to affect neurotrophic factor expression, which induces depression-like behavior. However, whether there are time-dependent changes in neurotrophic factor mRNA expression following stress remains unclear. In the present study, we tested whether chronic stress exposure induces long-term changes in depression-related behavior, serum corticosterone, and hippocampal proliferation as well as neurotrophic factor family mRNA levels, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3), and ciliary neurotrophic factor (CNTF), in the mouse hippocampus. The mRNA level of neurotrophic factors (BDNF, NGF, NT-3, and CNTF) was measured using the real-time PCR. The serum corticosterone level was evaluated by enzyme-linked immunosorbent assay, and, for each subject, the hippocampal proliferation was examined by 5-bromo-2-deoxyuridine immunostaining. Mice exhibited depression-like behavior in the forced-swim test (FST) and decreased BDNF mRNA and hippocampal proliferation in the middle of the stress exposure. After 15 days of stress exposure, we observed increased immobility in the FST, serum corticosterone levels, and BDNF mRNA levels and degenerated hippocampal proliferation, maintained for at least 2 weeks. Anhedonia-like behavior in the sucrose preference test and NGF mRNA levels were decreased following 15 days of stress. NGF mRNA levels were significantly higher 1 week after stress exposure. The current data demonstrate that chronic stress exposure induces prolonged BDNF and NGF mRNA changes and increases corticosterone levels and depression-like behavior in the FST, but does not alter other neurotrophic factors or performance in the sucrose preference test. FAU - Hashikawa, Naoya AU - Hashikawa N AD - Department of Life Science, Okayama University of Science, 1-1 Ridai-cho, Kita-ku, Okayama, 700-0005, Japan. FAU - Ogawa, Takumi AU - Ogawa T FAU - Sakamoto, Yusuke AU - Sakamoto Y FAU - Ogawa, Mami AU - Ogawa M FAU - Matsuo, Yumi AU - Matsuo Y FAU - Zamami, Yoshito AU - Zamami Y FAU - Hashikawa-Hobara, Narumi AU - Hashikawa-Hobara N LA - eng GR - D1DA31340/DA/NIDA NIH HHS/United States GR - R01DA23979/DA/NIDA NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20150328 PL - United States TA - Cell Mol Neurobiol JT - Cellular and molecular neurobiology JID - 8200709 RN - 0 (Nerve Growth Factors) RN - 0 (RNA, Messenger) RN - W980KJ009P (Corticosterone) SB - IM MH - Animals MH - Behavior, Animal/*physiology MH - Cell Proliferation MH - Chronic Disease MH - Corticosterone/blood MH - Dentate Gyrus/pathology MH - Hippocampus/pathology MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Nerve Growth Factors/*genetics/metabolism MH - RNA, Messenger/metabolism MH - *Stress, Psychological/genetics/metabolism/pathology/physiopathology MH - Time Factors EDAT- 2015/03/31 06:00 MHDA- 2016/04/21 06:00 CRDT- 2015/03/31 06:00 PHST- 2015/02/05 00:00 [received] PHST- 2015/03/07 00:00 [accepted] PHST- 2015/03/31 06:00 [entrez] PHST- 2015/03/31 06:00 [pubmed] PHST- 2016/04/21 06:00 [medline] AID - 10.1007/s10571-015-0174-x [doi] PST - ppublish SO - Cell Mol Neurobiol. 2015 Aug;35(6):807-17. doi: 10.1007/s10571-015-0174-x. Epub 2015 Mar 28.