PMID- 24211850 OWN - NLM STAT- MEDLINE DCOM- 20140816 LR - 20180816 IS - 1873-5118 (Electronic) IS - 0301-0082 (Linking) VI - 112 DP - 2014 Jan TI - Stress and trauma: BDNF control of dendritic-spine formation and regression. PG - 80-99 LID - S0301-0082(13)00116-0 [pii] LID - 10.1016/j.pneurobio.2013.10.005 [doi] AB - Chronic restraint stress leads to increases in brain derived neurotrophic factor (BDNF) mRNA and protein in some regions of the brain, e.g. the basal lateral amygdala (BLA) but decreases in other regions such as the CA3 region of the hippocampus and dendritic spine density increases or decreases in line with these changes in BDNF. Given the powerful influence that BDNF has on dendritic spine growth, these observations suggest that the fundamental reason for the direction and extent of changes in dendritic spine density in a particular region of the brain under stress is due to the changes in BDNF there. The most likely cause of these changes is provided by the stress initiated release of steroids, which readily enter neurons and alter gene expression, for example that of BDNF. Of particular interest is how glucocorticoids and mineralocorticoids tend to have opposite effects on BDNF gene expression offering the possibility that differences in the distribution of their receptors and of their downstream effects might provide a basis for the differential transcription of the BDNF genes. Alternatively, differences in the extent of methylation and acetylation in the epigenetic control of BDNF transcription are possible in different parts of the brain following stress. Although present evidence points to changes in BDNF transcription being the major causal agent for the changes in spine density in different parts of the brain following stress, steroids have significant effects on downstream pathways from the TrkB receptor once it is acted upon by BDNF, including those that modulate the density of dendritic spines. Finally, although glucocorticoids play a canonical role in determining BDNF modulation of dendritic spines, recent studies have shown a role for corticotrophin releasing factor (CRF) in this regard. There is considerable improvement in the extent of changes in spine size and density in rodents with forebrain specific knockout of CRF receptor 1 (CRFR1) even when the glucocorticoid pathways are left intact. It seems then that CRF does have a role to play in determining BDNF control of dendritic spines. CI - Copyright (c) 2013 Elsevier Ltd. All rights reserved. FAU - Bennett, M R AU - Bennett MR AD - The Brain and Mind Research Institute, The University of Sydney, Australia. Electronic address: max.bennett@sydney.edu.au. FAU - Lagopoulos, J AU - Lagopoulos J AD - The Brain and Mind Research Institute, The University of Sydney, Australia. LA - eng PT - Journal Article PT - Review DEP - 20131106 PL - England TA - Prog Neurobiol JT - Progress in neurobiology JID - 0370121 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 7171WSG8A2 (BDNF protein, human) SB - IM MH - Animals MH - Brain/*metabolism/*pathology MH - Brain Injuries/*metabolism/pathology MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Dendritic Spines/pathology/*physiology MH - Humans MH - Stress, Psychological/*metabolism/pathology OTO - NOTNLM OT - BDNF OT - BDNF receptor OT - CaMK2 OT - CaMKK OT - D2 OT - Dendrite OT - ERK OT - EphB OT - ErbB2 OT - ErbB4 OT - G-protein OT - GKAP OT - Gp OT - HOMER OT - IP3 OT - LIM kinase, phosphorylates ADF/cofilin OT - LIMK OT - N-methyl-d-aspartate OT - NMDA OT - NR1 OT - NR2A, NR2B, subunits of the NMDA receptor OT - NRG-1 OT - PAK OT - PDZ OT - PLCb OT - PP1 OT - PSD-95 OT - PTSD OT - RAC OT - RAS OT - ROCK OT - Rho GEF OT - Rho-GTPase OT - Rho-associated kinase OT - Rho-family GTPases, a subgroup of the superfamily of GTPases OT - RhoA OT - SFK OT - SHANK OT - Spines OT - Synapse OT - Trauma OT - TrkB OT - WASP OT - Wiskott Aldrich syndrome protein that triggers actin polymerization via Arp 2/3 complex OT - actin regulatory molecule OT - bPIX OT - brain derived neurotrophic factor OT - calcium calmodulin-dependent kinase 2 OT - calcium calmodulin-dependent protein kinase kinase OT - cofilin OT - dopamine D2 receptor OT - downstream effector of RAC (sometimes called P21-activated kinase) OT - ephrin receptor OT - extracellular signal-regulated kinases OT - guanine nucleotide exchange factor for RAC (GEF) OT - guanylate kinase-associated protein OT - inositol triphosphate OT - kalirin OT - neuregulin 1 OT - pCREB OT - phosphorylated cyclic AMP response element-binding protein OT - plexin A OT - postsynaptic density 95, a scaffolding protein OT - profilin OT - protein domain OT - protein lipase Cb OT - protein phosphatase 1 OT - receptor for Sema 3A OT - receptors for neuregulin OT - scaffolding molecule OT - scaffolding protein OT - sema 3A OT - semaphorin 3A OT - severs and depolymerizes ADPactin OT - src family kinase EDAT- 2013/11/12 06:00 MHDA- 2014/08/17 06:00 CRDT- 2013/11/12 06:00 PHST- 2013/07/10 00:00 [received] PHST- 2013/10/16 00:00 [revised] PHST- 2013/10/17 00:00 [accepted] PHST- 2013/11/12 06:00 [entrez] PHST- 2013/11/12 06:00 [pubmed] PHST- 2014/08/17 06:00 [medline] AID - S0301-0082(13)00116-0 [pii] AID - 10.1016/j.pneurobio.2013.10.005 [doi] PST - ppublish SO - Prog Neurobiol. 2014 Jan;112:80-99. doi: 10.1016/j.pneurobio.2013.10.005. Epub 2013 Nov 6.