PMID- 17447135
OWN - NLM
STAT- MEDLINE
DCOM- 20080122
LR  - 20181113
IS  - 0272-4340 (Print)
IS  - 0272-4340 (Linking)
VI  - 27
IP  - 5
DP  - 2007 Aug
TI  - Rapid activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) 
      signaling pathway by electroconvulsive shock in the rat prefrontal cortex is not 
      associated with TrkB neurotrophin receptor activation.
PG  - 585-94
AB  - 1. Emerging evidence indicates that brain-derived neurotrophic factor (BDNF) and 
      its receptor TrkB play important roles in the mechanism of action of 
      electroconvulsive shock (ECS) treatment. ECS produces a significant increase in 
      brain BDNF synthesis together with a variety of neuroplastic changes including 
      neurogenesis and axonal sprouting in the rodent brain, which is believed to be 
      associated to the antidepressant effect of ECS. ERK1/2 (extracellular 
      signal-regulated kinase-1/2) and Akt (protein kinase B), both intracellular 
      signaling molecules being linked to neurotrophin signaling and synthesis, are 
      important pathways triggered by TrkB autophosphorylation. 2. We have previously 
      observed that chemical antidepressants induce a rapid activation of TrkB 
      signaling in the rodent prefrontal cortex (PFC), which is likely a consequence of 
      the stimulatory effect of antidepressants on BDNF synthesis. However, it is not 
      known whether ECS triggers TrkB autophosphorylation and if any ECS-induced effect 
      on TrkB function may be associated with the activation of the ERK1/2 and Akt 
      pathways. 3. The present study assayed the phosphorylation levels of TrkB, 
      ERK1/2, and Akt in the PFC of sham and ECS-treated rats. While the TrkB 
      autophosphorylation (pTrkB) levels were decreased 30 min after both acute and 
      chronic ECS, no change in pTrkB levels were observed at any other time points 
      measured. In contrast, acute but not chronic ECS, transiently induced a very 
      rapid and robust hyperphosphorylation of ERK1/2. Akt phosphorylation levels 
      remained unchanged following acute or chronic ECS. Hence, although ECS 
      effectively stimulates the ERK1/2 pathway in the PFC, this effect does not appear 
      to involve upstream activation of TrkB.
FAU - Hansen, Henrik H
AU  - Hansen HH
AD  - Department of Translational Neurobiology, Neurosearch A/S, Pederstrupvej 93, 
      DK-2750, Ballerup, Copenhagen, Denmark. heh@neurosearch.dk
FAU - Rantamaki, Tomi P J
AU  - Rantamaki TP
FAU - Larsen, Marianne H
AU  - Larsen MH
FAU - Woldbye, David P D
AU  - Woldbye DP
FAU - Mikkelsen, Jens D
AU  - Mikkelsen JD
FAU - Castren, Eero H
AU  - Castren EH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
MH  - Animals
MH  - *Electroshock
MH  - MAP Kinase Signaling System/physiology
MH  - Male
MH  - Mitogen-Activated Protein Kinase 1/*metabolism
MH  - Mitogen-Activated Protein Kinase 3/*metabolism
MH  - Oncogene Protein v-akt/metabolism
MH  - Phosphorylation
MH  - Prefrontal Cortex/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/*metabolism
EDAT- 2007/04/21 09:00
MHDA- 2008/01/23 09:00
CRDT- 2007/04/21 09:00
PHST- 2007/01/22 00:00 [received]
PHST- 2007/03/23 00:00 [accepted]
PHST- 2007/04/21 09:00 [pubmed]
PHST- 2008/01/23 09:00 [medline]
PHST- 2007/04/21 09:00 [entrez]
AID - 10.1007/s10571-007-9145-1 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2007 Aug;27(5):585-94. doi: 10.1007/s10571-007-9145-1.