PMID- 23022538 OWN - NLM STAT- MEDLINE DCOM- 20131017 LR - 20211021 IS - 1873-7544 (Electronic) IS - 0306-4522 (Print) IS - 0306-4522 (Linking) VI - 239 DP - 2013 Jun 3 TI - Are BDNF and glucocorticoid activities calibrated? PG - 173-95 LID - S0306-4522(12)00920-7 [pii] LID - 10.1016/j.neuroscience.2012.09.017 [doi] AB - One hypothesis to account for the onset and severity of neurological disorders is the loss of trophic support. Indeed, changes in the levels and activities of brain-derived neurotrophic factor (BDNF) occur in numerous neurodegenerative and neuropsychiatric diseases. A deficit promotes vulnerability whereas a gain of function facilitates recovery by enhancing survival, synapse formation and synaptic plasticity. Implementation of 'BDNF therapies', however, faces numerous methodological and pharmacokinetic issues. Identifying BDNF mimetics that activate the BDNF receptor or downstream targets of BDNF signaling represent an alternative approach. One mechanism that shows great promise is to study the interplay of BDNF and glucocorticoid hormones, a major class of natural steroid secreted during stress reactions and in synchrony with circadian rhythms. While small amounts of glucocorticoids support normal brain function, excess stimulation by these steroid hormones precipitates stress-related affective disorders. To date, however, because of the paucity of knowledge of underlying cellular mechanisms, deleterious effects of glucocorticoids are not prevented following extreme stress. In the present review, we will discuss the complementary roles shared by BDNF and glucocorticoids in synaptic plasticity, and delineate possible signaling mechanisms mediating these effects. CI - Copyright (c) 2012 IBRO. All rights reserved. FAU - Jeanneteau, F AU - Jeanneteau F AD - Skirball Institute of Biomolecular Medicine, Department of Cell Biology, NYU School of Medicine, New York, NY 10016, USA. Freddy.jeanneteau@med.nyu.edu FAU - Chao, M V AU - Chao MV LA - eng GR - MH086651/MH/NIMH NIH HHS/United States GR - NS21072/NS/NINDS NIH HHS/United States GR - R01 NS021072/NS/NINDS NIH HHS/United States GR - R01 AG025970/AG/NIA NIH HHS/United States GR - R01 MH086651/MH/NIMH NIH HHS/United States GR - R56 NS021072/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20120926 PL - United States TA - Neuroscience JT - Neuroscience JID - 7605074 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Glucocorticoids) SB - IM MH - Animals MH - Brain/*metabolism MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Glucocorticoids/*metabolism MH - Humans MH - Neuronal Plasticity/*physiology MH - Neurons/metabolism MH - Signal Transduction/*physiology PMC - PMC3581703 MID - NIHMS410699 EDAT- 2012/10/02 06:00 MHDA- 2013/10/18 06:00 PMCR- 2014/06/03 CRDT- 2012/10/02 06:00 PHST- 2012/07/02 00:00 [received] PHST- 2012/09/04 00:00 [revised] PHST- 2012/09/06 00:00 [accepted] PHST- 2012/10/02 06:00 [entrez] PHST- 2012/10/02 06:00 [pubmed] PHST- 2013/10/18 06:00 [medline] PHST- 2014/06/03 00:00 [pmc-release] AID - S0306-4522(12)00920-7 [pii] AID - 10.1016/j.neuroscience.2012.09.017 [doi] PST - ppublish SO - Neuroscience. 2013 Jun 3;239:173-95. doi: 10.1016/j.neuroscience.2012.09.017. Epub 2012 Sep 26.