PMID- 16905274
OWN - NLM
STAT- MEDLINE
DCOM- 20070405
LR  - 20091119
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 68
IP  - 3
DP  - 2007
TI  - TrkB partial agonists: potential treatment strategy for major depression.
PG  - 674-6
AB  - Brain-derived neurotrophic factor (BDNF) regulates a wide variety of processes in 
      the nervous system, including neural development, function and survival, through 
      activation of the tyrosine kinase B receptor (TrkB). Evidence suggests that low 
      central BDNF activity, especially in the hippocampus, may play a pivotal role in 
      the pathophysiology of major depression, and that agents that can increase 
      BDNF-TrkB pathway signaling may be therapeutic for this disease. However, recent 
      studies showed that increased BDNF activity in the mesolimbic region may cause a 
      depressed state. A partial agonist is an agent that elicits a maximum response 
      that is less than that of an agonist and acts as an antagonist in the presence of 
      excess full agonist. Recently some small peptides have been synthesized that act 
      as TrkB partial agonists. Since BDNF might be pro-depressive in the mesolimbic 
      system and anti-depressive in the hippocampus region, it is proposed that these 
      peptides or other partial TrkB agonists may provide a novel strategy for the 
      treatment of major depression, which may be associated with BDNF-TrkB 
      hypofunction in hippocampus and/or hyperfunction in the mesolimbic system. 
      Furthermore, given the potential imbalance of BDNF in specific brain regions in 
      major depression, selection of agents with maximal hippocampus/mesolimbic BDNF 
      activation ratio could be of importance in the development of novel 
      antidepressants.
FAU - Tsai, Shih-Jen
AU  - Tsai SJ
AD  - Department of Psychiatry, Taipei Veterans General Hospital, 201 Shih-Pai Road, 
      Sec. 2, 11217 Taipei, Taiwan. sjtsai@vghtpe.gov.tw
LA  - eng
PT  - Journal Article
DEP - 20060814
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/physiology
MH  - Depressive Disorder/*therapy
MH  - Electroconvulsive Therapy
MH  - Receptor, trkB/agonists/*physiology
EDAT- 2006/08/15 09:00
MHDA- 2007/04/06 09:00
CRDT- 2006/08/15 09:00
PHST- 2006/06/10 00:00 [received]
PHST- 2006/06/13 00:00 [accepted]
PHST- 2006/08/15 09:00 [pubmed]
PHST- 2007/04/06 09:00 [medline]
PHST- 2006/08/15 09:00 [entrez]
AID - S0306-9877(06)00472-5 [pii]
AID - 10.1016/j.mehy.2006.06.019 [doi]
PST - ppublish
SO  - Med Hypotheses. 2007;68(3):674-6. doi: 10.1016/j.mehy.2006.06.019. Epub 2006 Aug 
      14.