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Article: Physical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin

TitlePhysical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin
Authors
Issue Date2014
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings of the National Academy of Sciences, 2014, v. 111 n. 44, p. 15810-15815 How to Cite?
AbstractAdiponectin (ADN) is an adipocyte-secreted protein with insulin-sensitizing, antidiabetic, antiinflammatory, and antiatherogenic properties. Evidence is also accumulating that ADN has neuroprotective activities, yet the underlying mechanism remains elusive. Here we show that ADN could pass through the blood-brain barrier, and elevating its levels in the brain increased cell proliferation and decreased depression-like behaviors. ADN deficiency did not reduce the basal hippocampal neurogenesis or neuronal differentiation but diminished the effectiveness of exercise in increasing hippocampal neurogenesis. Furthermore, exercise-induced reduction in depression-like behaviors was abrogated in ADN-deficient mice, and this impairment in ADN-deficient mice was accompanied by defective running-induced phosphorylation of AMP-activated protein kinase (AMPK) in the hippocampal tissue. In vitro analyses indicated that ADN itself could increase cell proliferation of both hippocampal progenitor cells and Neuro2a neuroblastoma cells. The neurogenic effects of ADN were mediated by the ADN receptor 1 (ADNR1), because siRNA targeting ADNR1, but not ADNR2, inhibited the capacity of ADN to enhance cell proliferation. These data suggest that adiponectin may play a significant role in mediating the effects of exercise on hippocampal neurogenesis and depression, possibly by activation of the ADNR1/AMPK signaling pathways, and also raise the possibility that adiponectin and its agonists may represent a promising therapeutic treatment for depression.
Persistent Identifierhttp://hdl.handle.net/10722/206898
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorYau, SY-
dc.contributor.authorLi, A-
dc.contributor.authorHoo, RLC-
dc.contributor.authorChing, YP-
dc.contributor.authorChristie, B. R.-
dc.contributor.authorLee, TMC-
dc.contributor.authorXu, A-
dc.contributor.authorSo, KF-
dc.date.accessioned2014-12-02T12:04:53Z-
dc.date.available2014-12-02T12:04:53Z-
dc.date.issued2014-
dc.identifier.citationProceedings of the National Academy of Sciences, 2014, v. 111 n. 44, p. 15810-15815-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/206898-
dc.description.abstractAdiponectin (ADN) is an adipocyte-secreted protein with insulin-sensitizing, antidiabetic, antiinflammatory, and antiatherogenic properties. Evidence is also accumulating that ADN has neuroprotective activities, yet the underlying mechanism remains elusive. Here we show that ADN could pass through the blood-brain barrier, and elevating its levels in the brain increased cell proliferation and decreased depression-like behaviors. ADN deficiency did not reduce the basal hippocampal neurogenesis or neuronal differentiation but diminished the effectiveness of exercise in increasing hippocampal neurogenesis. Furthermore, exercise-induced reduction in depression-like behaviors was abrogated in ADN-deficient mice, and this impairment in ADN-deficient mice was accompanied by defective running-induced phosphorylation of AMP-activated protein kinase (AMPK) in the hippocampal tissue. In vitro analyses indicated that ADN itself could increase cell proliferation of both hippocampal progenitor cells and Neuro2a neuroblastoma cells. The neurogenic effects of ADN were mediated by the ADN receptor 1 (ADNR1), because siRNA targeting ADNR1, but not ADNR2, inhibited the capacity of ADN to enhance cell proliferation. These data suggest that adiponectin may play a significant role in mediating the effects of exercise on hippocampal neurogenesis and depression, possibly by activation of the ADNR1/AMPK signaling pathways, and also raise the possibility that adiponectin and its agonists may represent a promising therapeutic treatment for depression.-
dc.languageeng-
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org-
dc.relation.ispartofProceedings of the National Academy of Sciences-
dc.titlePhysical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin-
dc.typeArticle-
dc.identifier.emailYau, SY: yausukyu@hku.hk-
dc.identifier.emailHoo, RLC: rubyhoo@hkucc.hku.hk-
dc.identifier.emailChing, YP: ypching@hku.hk-
dc.identifier.emailLee, TMC: tmclee@hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailSo, KF: hrmaskf@hku.hk-
dc.identifier.authorityHoo, RLC=rp01334-
dc.identifier.authorityChing, YP=rp00469-
dc.identifier.authorityLee, TMC=rp00564-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authoritySo, KF=rp00329-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1415219111-
dc.identifier.pmid25331877-
dc.identifier.pmcidPMC4226125-
dc.identifier.hkuros241512-
dc.identifier.hkuros241669-
dc.identifier.volume111-
dc.identifier.issue44-
dc.identifier.spage15810-
dc.identifier.epage15815-
dc.publisher.placeUnited States-

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