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Article: Sustained running in rats administered corticosterone prevents the development of depressive behaviors and enhances hippocampal neurogenesis and synaptic plasticity without increasing neurotrophic factor levels

TitleSustained running in rats administered corticosterone prevents the development of depressive behaviors and enhances hippocampal neurogenesis and synaptic plasticity without increasing neurotrophic factor levels
Authors
KeywordsBrain-derived neurotrophic factor
Depression-like behavior
Hippocampal neurogenesis
Insulin-like growth factor
Physical exercise
Issue Date2014
PublisherCognizant Communication Corp. The Journal's web site is located at https://www.cognizantcommunication.com/journal-titles/cell-transplantation
Citation
Cell Transplantation, 2014, v. 23 n. 4-5, p. 481-492 How to Cite?
AbstractWe have previously shown that voluntary running acts as an anxiolytic and ameliorates deficits in hippocampal neurogenesis and spatial learning. It also reduces depression-like behaviors that are normally observed in rats that were administered either low (30 mg/kg) or moderate (40 mg/kg) doses of corticosterone (CORT). However, the protective effects of running were absent in rats treated with a high (50 mg/kg) dose of CORT. We examined whether allowing animals to exercise for 2 weeks prior and/or concurrently with the administration of 50 mg/kg CORT treatment could have similar protective effects. We examined hippocampal neurogenesis using immunohistochemical staining of proliferative and survival cells with the thymidine analogs (BrdU, CIdU, and IdU). In addition, we monitored synaptic protein expression and quantified the levels of neurotrophic factors in these animals as well as performing behavioral analyses (forced swim test and sucrose preference test). Our results indicate that the depressive phenotype and reductions in neurogenesis that normally accompany high CORT administration could only be prevented by allowing animals to exercise both prior to and concurrently with the CORT administration period. These animals also showed increases in both synaptophysin and PSD-95 protein levels, but surprisingly, neither brain-derived neurotrophic factor (BDNF) nor insulin-like growth factor 1 (IGF-1) levels were increased in these animals. The results suggest that persistent exercise can strengthen resilience to stress by promoting hippocampal neurogenesis and increasing synaptic protein levels, thereby reducing the deleterious effects of stress.
Persistent Identifierhttp://hdl.handle.net/10722/198258
ISSN
2015 Impact Factor: 3.427
2015 SCImago Journal Rankings: 1.161
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYau, SYen_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorZhang, EDen_US
dc.contributor.authorChristie, BRen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorLee, TMCen_US
dc.contributor.authorSo, KFen_US
dc.date.accessioned2014-06-25T02:57:30Z-
dc.date.available2014-06-25T02:57:30Z-
dc.date.issued2014en_US
dc.identifier.citationCell Transplantation, 2014, v. 23 n. 4-5, p. 481-492en_US
dc.identifier.issn0963-6897-
dc.identifier.urihttp://hdl.handle.net/10722/198258-
dc.description.abstractWe have previously shown that voluntary running acts as an anxiolytic and ameliorates deficits in hippocampal neurogenesis and spatial learning. It also reduces depression-like behaviors that are normally observed in rats that were administered either low (30 mg/kg) or moderate (40 mg/kg) doses of corticosterone (CORT). However, the protective effects of running were absent in rats treated with a high (50 mg/kg) dose of CORT. We examined whether allowing animals to exercise for 2 weeks prior and/or concurrently with the administration of 50 mg/kg CORT treatment could have similar protective effects. We examined hippocampal neurogenesis using immunohistochemical staining of proliferative and survival cells with the thymidine analogs (BrdU, CIdU, and IdU). In addition, we monitored synaptic protein expression and quantified the levels of neurotrophic factors in these animals as well as performing behavioral analyses (forced swim test and sucrose preference test). Our results indicate that the depressive phenotype and reductions in neurogenesis that normally accompany high CORT administration could only be prevented by allowing animals to exercise both prior to and concurrently with the CORT administration period. These animals also showed increases in both synaptophysin and PSD-95 protein levels, but surprisingly, neither brain-derived neurotrophic factor (BDNF) nor insulin-like growth factor 1 (IGF-1) levels were increased in these animals. The results suggest that persistent exercise can strengthen resilience to stress by promoting hippocampal neurogenesis and increasing synaptic protein levels, thereby reducing the deleterious effects of stress.-
dc.languageengen_US
dc.publisherCognizant Communication Corp. The Journal's web site is located at https://www.cognizantcommunication.com/journal-titles/cell-transplantation-
dc.relation.ispartofCell Transplantationen_US
dc.rightsCell Transplantation. Copyright © Cognizant Communication Corp.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectBrain-derived neurotrophic factor-
dc.subjectDepression-like behavior-
dc.subjectHippocampal neurogenesis-
dc.subjectInsulin-like growth factor-
dc.subjectPhysical exercise-
dc.titleSustained running in rats administered corticosterone prevents the development of depressive behaviors and enhances hippocampal neurogenesis and synaptic plasticity without increasing neurotrophic factor levelsen_US
dc.typeArticleen_US
dc.identifier.emailYau, SY: yausukyu@hku.hken_US
dc.identifier.emailZhang, ED: endongz@hkusua.hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailLee, TMC: tmclee@hku.hken_US
dc.identifier.emailSo, KF: hrmaskf@hku.hken_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityLee, TMC=rp00564en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3727/096368914X678490-
dc.identifier.pmid24816445-
dc.identifier.scopuseid_2-s2.0-84900389076-
dc.identifier.hkuros229260en_US
dc.identifier.hkuros239684-
dc.identifier.hkuros239020-
dc.identifier.volume23en_US
dc.identifier.issue4-5-
dc.identifier.spage481en_US
dc.identifier.epage492en_US
dc.identifier.isiWOS:000333884900009-
dc.publisher.placeUnited States-

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