PMID- 17852404
OWN - NLM
STAT- MEDLINE
DCOM- 20071213
LR  - 20131121
IS  - 0897-7194 (Print)
IS  - 0897-7194 (Linking)
VI  - 25
IP  - 2
DP  - 2007 Apr
TI  - Running exercise- and antidepressant-induced increases in growth and 
      survival-associated signaling molecules are IGF-dependent.
PG  - 118-31
AB  - It is known that physical exercise increases hippocampal brain-derived 
      neurotrophic factor (BDNF) mRNA and protein, as well as the expression of several 
      pro-survival signaling proteins and that many of these effects depend on the 
      uptake of peripheral insulin-like growth factor-1 (IGF-1) into the CNS. Because 
      treatment with antidepressants has similar effects upon neurotrophin expression, 
      we investigated whether antidepressant-induced BDNF changes also depend on IGF-1 
      uptake, as well as whether IGF-1 plays a role in the 
      exercise/antidepressant-induced expression of molecules associated with 
      plasticity/growth (GAP-43, SCG-10) and the intracellular activation of molecules 
      associated with neuronal survival (Akt, ERK1/2). We evaluated the effects of a 
      well known monoamine oxidase inhibitor, tranylcypromine, on BDNF mRNA and protein 
      levels and phospho-Akt and phospho-ERK1/2 immunoreactivity, both with and without 
      systemic blockade of IGF-1 uptake through the use of an antiserum raised against 
      IGF-1. Anti-IGF-1 reversed the increase in BDNF mRNA and protein elicited by 
      exercise as well as tranylcypromine. Exercise also significantly enhanced 
      transcription of axon growth protein, GAP-43, an effect that was also evidenced 
      to be IGF-1-dependent. The combination of exercise-plus-tranylcypromine also 
      increased several cell survival signaling measures, but the BDNF changes 
      associated with the combination treatment appeared to be independent of IGF-1 
      uptake. Together, these results indicate that the uptake of peripheral IGF-1 in 
      the CNS is essential for antidepressant- as well as exercise-induced enhancement 
      in hippocampal BDNF expression and thus, enhanced hippocampal neuronal survival 
      and plasticity.
FAU - Chen, Michael J
AU  - Chen MJ
AD  - Department of Biological Sciences, California State University, 5151 State 
      University Drive, Los Angeles, CA 90032, USA. mchen@calstatela.edu
FAU - Russo-Neustadt, Amelia A
AU  - Russo-Neustadt AA
LA  - eng
GR  - MH 59776/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Growth Factors
JT  - Growth factors (Chur, Switzerland)
JID - 9000468
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Monoamine Oxidase Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Somatomedins)
RN  - 3E3V44J4Z9 (Tranylcypromine)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents/*therapeutic use
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cell Proliferation
MH  - Hippocampus/metabolism
MH  - In Situ Hybridization
MH  - Male
MH  - Models, Biological
MH  - Monoamine Oxidase Inhibitors/pharmacology
MH  - Neurons/metabolism
MH  - *Physical Conditioning, Animal
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Running
MH  - Signal Transduction
MH  - Somatomedins/*metabolism
MH  - Tranylcypromine/pharmacology
EDAT- 2007/09/14 09:00
MHDA- 2007/12/14 09:00
CRDT- 2007/09/14 09:00
PHST- 2007/09/14 09:00 [pubmed]
PHST- 2007/12/14 09:00 [medline]
PHST- 2007/09/14 09:00 [entrez]
AID - 781568373 [pii]
AID - 10.1080/08977190701602329 [doi]
PST - ppublish
SO  - Growth Factors. 2007 Apr;25(2):118-31. doi: 10.1080/08977190701602329.