PMID- 17949819
OWN - NLM
STAT- MEDLINE
DCOM- 20080311
LR  - 20220309
IS  - 0163-7258 (Print)
IS  - 0163-7258 (Linking)
VI  - 117
IP  - 1
DP  - 2008 Jan
TI  - Brain-derived neurotrophic factor and its receptor tropomyosin-related kinase B 
      in the mechanism of action of antidepressant therapies.
PG  - 30-51
AB  - The focus of this review is to critically examine and review the literature on 
      the role of brain-derived neurotrophic factor (BDNF) and its primary receptor, 
      tropomyosin-related kinase B (TrkB), in the actions of pharmacologically diverse 
      antidepressant treatments for depression. This will include a review of the 
      studies on the regulation of BDNF and TrkB by different types of antidepressant 
      drug treatments and animal in models of depression, as well as altered levels of 
      BDNF and TrkB in the blood and postmortem brain of patients with depression. 
      Results from clinical and basic studies have demonstrated that stress and 
      depression decrease BDNF expression and neurogenesis and antidepressant treatment 
      reverses or blocks these effects, leading to the neurotrophic hypothesis of 
      depression. Clinical studies demonstrate an association between BDNF levels and 
      several disorders, including depression, epilepsy, bipolar disorder, Parkinson's 
      and Alzheimer's diseases. Physical activity and diet exert neurotrophic effects 
      and positively modulate BDNF levels. A common single nucleotide polymorphism 
      (SNP) in the BDNF gene, a methionine substitution for valine, is associated with 
      alterations in brain anatomy and memory, but what role it has in clinical 
      disorders is unclear. Findings suggest that early childhood events and adult 
      stress produce neurodegenerative alterations in the brain that can eventually 
      cause breakdown of information processing in the neuronal networks regulating 
      mood. Antidepressant treatments elevate activity-dependent neuronal plasticity by 
      activating BDNF, thereby gradually restoring network function and ultimately 
      mood.
FAU - Kozisek, Megan E
AU  - Kozisek ME
AD  - Department of Pharmacology and Experimental Neuroscience, University of Nebraska 
      Medical Center, Omaha, NE 68198-5800, United States. megankozisek@yahoo.com
FAU - Middlemas, David
AU  - Middlemas D
FAU - Bylund, David B
AU  - Bylund DB
LA  - eng
GR  - MH064772/MH/NIMH 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 - 20070815
PL  - England
TA  - Pharmacol Ther
JT  - Pharmacology & therapeutics
JID - 7905840
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Antidepressive Agents/*pharmacology
MH  - Brain-Derived Neurotrophic Factor/drug effects/*metabolism
MH  - Child
MH  - Clinical Trials as Topic
MH  - Depressive Disorder/drug therapy
MH  - Disease Models, Animal
MH  - Drug Delivery Systems
MH  - Humans
MH  - Mood Disorders/drug therapy
MH  - Receptor, trkB/drug effects/*metabolism
RF  - 209
EDAT- 2007/10/24 09:00
MHDA- 2008/03/12 09:00
CRDT- 2007/10/24 09:00
PHST- 2007/07/24 00:00 [received]
PHST- 2007/07/24 00:00 [accepted]
PHST- 2007/10/24 09:00 [pubmed]
PHST- 2008/03/12 09:00 [medline]
PHST- 2007/10/24 09:00 [entrez]
AID - S0163-7258(07)00152-0 [pii]
AID - 10.1016/j.pharmthera.2007.07.001 [doi]
PST - ppublish
SO  - Pharmacol Ther. 2008 Jan;117(1):30-51. doi: 10.1016/j.pharmthera.2007.07.001. 
      Epub 2007 Aug 15.