PMID- 23747574 OWN - NLM STAT- MEDLINE DCOM- 20140806 LR - 20220321 IS - 1873-7064 (Electronic) IS - 0028-3908 (Print) IS - 0028-3908 (Linking) VI - 76 Pt C IP - 0 0 DP - 2014 Jan TI - Synaptic regulation of affective behaviors; role of BDNF. PG - 684-95 LID - S0028-3908(13)00148-2 [pii] LID - 10.1016/j.neuropharm.2013.04.011 [doi] AB - Brain derived neurotrophic factor (BDNF), a neurotrophin essential for nervous system development and synaptic plasticity, has been found to have a significant influence on affective behaviors. The notion that an impairment in BDNF signaling might be involved in affective disorders is originated primarily from the opposing effects of antidepressants and stress on BDNF signaling. Antidepressants enhance BDNF signaling and synaptic plasticity. On the other hand, negative environmental factors such as severe stress suppress BDNF signaling, impair synaptic activity and increase susceptibility to affective disorders. Postmortem studies provided strong support for decreased BDNF signaling in depressive disorders. Remarkably, studies in humans with a single nucleotide polymorphism in the BDNF gene, the BDNF Val66Met which affects regulated release of BDNF, showed profound deficits in hippocampal and prefrontal cortical (PFC) plasticity and cognitive behaviors. BDNF regulates synaptic mechanisms responsible for various cognitive processes including attenuation of aversive memories, a key process in the regulation of affective behaviors. The unique role of BDNF in cognitive and affective behaviors suggests that cognitive deficits due to altered BDNF signaling might underlie affective disorders. Understanding how BDNF modulates synapses in neural circuits relevant to affective behaviors, particularly the medial prefrontal cortical (mPFC)-hippocampus-amygdala pathway, and its interaction with development, sex, and environmental risk factors might shed light on potential therapeutic targets for affective disorders. This article is part of the Special Issue entitled 'BDNF Regulation of Synaptic Structure, Function, and Plasticity'. CI - Copyright (c) 2013 Elsevier Ltd. All rights reserved. FAU - Ninan, Ipe AU - Ninan I AD - Department of Psychiatry, NYU School of Medicine, SKI 5-3, 540 1st Ave, NY 10016, United States. Electronic address: Ipe.Ninan@nyumc.org. LA - eng GR - R01 MH096899/MH/NIMH NIH HHS/United States GR - R56 MH096899/MH/NIMH NIH HHS/United States GR - R01 MH96899/MH/NIMH NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Review DEP - 20130606 PL - England TA - Neuropharmacology JT - Neuropharmacology JID - 0236217 RN - 0 (Brain-Derived Neurotrophic Factor) SB - IM MH - Affect/*physiology MH - Animals MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Humans MH - Mood Disorders/*metabolism/pathology MH - Neuronal Plasticity/*physiology MH - Synapses/*metabolism PMC - PMC3825795 MID - NIHMS491311 OTO - NOTNLM OT - Affective behaviors OT - BDNF OT - Medial prefrontal cortex OT - Synaptic plasticity EDAT- 2013/06/12 06:00 MHDA- 2014/08/07 06:00 PMCR- 2015/01/01 CRDT- 2013/06/11 06:00 PHST- 2013/03/02 00:00 [received] PHST- 2013/03/31 00:00 [revised] PHST- 2013/04/02 00:00 [accepted] PHST- 2013/06/11 06:00 [entrez] PHST- 2013/06/12 06:00 [pubmed] PHST- 2014/08/07 06:00 [medline] PHST- 2015/01/01 00:00 [pmc-release] AID - S0028-3908(13)00148-2 [pii] AID - 10.1016/j.neuropharm.2013.04.011 [doi] PST - ppublish SO - Neuropharmacology. 2014 Jan;76 Pt C(0 0):684-95. doi: 10.1016/j.neuropharm.2013.04.011. Epub 2013 Jun 6.