PMID- 24875178
OWN - NLM
STAT- MEDLINE
DCOM- 20180126
LR  - 20211021
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 282
DP  - 2014 Dec 12
TI  - Neurotrophins in the ventral tegmental area: Role in social stress, mood 
      disorders and drug abuse.
PG  - 122-38
LID - S0306-4522(14)00420-5 [pii]
LID - 10.1016/j.neuroscience.2014.05.028 [doi]
AB  - This review discusses the impact of neurotrophins and other trophic factors, 
      including fibroblast growth factor and glial cell line-derived neurotrophic 
      factor, on mood disorders, weight regulation and drug abuse, with an emphasis on 
      stress- and drug-induced changes in the ventral tegmental area (VTA). 
      Neurotrophins, comprising nerve growth factor, brain-derived neurotrophic factor 
      (BDNF), and neurotrophins 3 and 4/5 play important roles in neuronal plasticity 
      and the development of different psychopathologies. In the VTA, most research has 
      focused on the role of BDNF, because other neurotrophins are not found there in 
      significant quantities. BDNF originating in the VTA provides trophic support to 
      dopamine neurons. The diverse intracellular signaling pathways activated by BDNF 
      may underlie precise physiological functions specific to the VTA. In general, VTA 
      BDNF expression increases after psychostimulant exposures, and enhanced BDNF 
      level in the VTA facilitates psychostimulant effects. The impact of VTA BDNF on 
      the behavioral effects of psychostimulants relies primarily on its action within 
      the mesocorticolimbic circuit. In the case of opiates, VTA BDNF expression and 
      effects seem to be dependent on whether an animal is drug-naive or has a history 
      of drug use, only the latter of which is related to dopamine mechanisms. Social 
      defeat stress that is continuous in mice or intermittent in rats increases VTA 
      BDNF expression, and is associated with depressive and social avoidance 
      behaviors. Intermittent social defeat stress induces persistent VTA BDNF 
      expression that triggers psychostimulant cross-sensitization. Understanding the 
      cellular and molecular substrates of neurotrophin effects may lead to novel 
      therapeutic approaches for the prevention and treatment of substance use and mood 
      disorders.
CI  - Copyright (c) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Nikulina, E M
AU  - Nikulina EM
AD  - Department of Basic Medical Sciences, University of Arizona College of Medicine, 
      Phoenix, AZ, USA. Electronic address: nikulina@email.arizona.edu.
FAU - Johnston, C E
AU  - Johnston CE
AD  - Department of Basic Medical Sciences, University of Arizona College of Medicine, 
      Phoenix, AZ, USA; Interdisciplinary Neuroscience Program, Arizona State 
      University, Tempe, AZ, USA.
FAU - Wang, J
AU  - Wang J
AD  - Interdisciplinary Neuroscience Program, Arizona State University, Tempe, AZ, USA.
FAU - Hammer, R P Jr
AU  - Hammer RP Jr
AD  - Department of Basic Medical Sciences, University of Arizona College of Medicine, 
      Phoenix, AZ, USA; Interdisciplinary Neuroscience Program, Arizona State 
      University, Tempe, AZ, USA; Department of Pharmacology and Department of 
      Psychiatry, University of Arizona College of Medicine, Tucson, AZ, USA.
LA  - eng
GR  - R01 DA026451/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20140527
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Behavior, Animal/*physiology
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Mood Disorders/*metabolism
MH  - Stress, Psychological/*metabolism
MH  - Substance-Related Disorders/*metabolism
MH  - Ventral Tegmental Area/*metabolism
PMC - PMC4246027
MID - NIHMS601485
OTO - NOTNLM
OT  - BDNF
OT  - cross-sensitization
OT  - depression
OT  - drug abuse
OT  - social stress
EDAT- 2014/05/31 06:00
MHDA- 2014/05/31 06:01
PMCR- 2015/11/27
CRDT- 2014/05/31 06:00
PHST- 2014/01/30 00:00 [received]
PHST- 2014/05/04 00:00 [revised]
PHST- 2014/05/11 00:00 [accepted]
PHST- 2014/05/31 06:00 [entrez]
PHST- 2014/05/31 06:00 [pubmed]
PHST- 2014/05/31 06:01 [medline]
PHST- 2015/11/27 00:00 [pmc-release]
AID - S0306-4522(14)00420-5 [pii]
AID - 10.1016/j.neuroscience.2014.05.028 [doi]
PST - ppublish
SO  - Neuroscience. 2014 Dec 12;282:122-38. doi: 10.1016/j.neuroscience.2014.05.028. 
      Epub 2014 May 27.