PMID- 18511210
OWN - NLM
STAT- MEDLINE
DCOM- 20080829
LR  - 20161124
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 154
IP  - 3
DP  - 2008 Jun 26
TI  - Status epilepticus induces a TrkB to p75 neurotrophin receptor switch and 
      increases brain-derived neurotrophic factor interaction with p75 neurotrophin 
      receptor: an initial event in neuronal injury induction.
PG  - 978-93
LID - 10.1016/j.neuroscience.2008.04.038 [doi]
AB  - In neuronal cultures it has been demonstrated that neurotrophins can elicit 
      neuronal death through the p75 neurotrophic receptor (p75ntr) in the absence of 
      concomitant Trk signaling. However, it was suggested that p75ntr induces neuronal 
      death after status epilepticus (SE) in neuronal populations that express 
      relatively high quantities of tropomyosin receptor kinase B (TrkB). Here, using 
      Western blot and immunohistochemistry analyses in the hippocampus, we found that 
      3-h SE caused a remarkable decrease in TrkB expression and phosphorylation, and a 
      significant increase in p75ntr. TrkB modification occurs before the 
      overexpression of the tumor suppressor protein p53, accompanies the cell damage 
      taking place in the dentate gyrus, and precedes the CA1 neuronal injury as 
      assessed by Fluoro-Jade B and Nissl staining. Co-immunoprecipitation of 
      brain-derived neurotrophic factor (BDNF) or its immature form proBDNF showed 
      increased interaction with p75ntr after its binding to TrkB was reduced. 
      Interestingly, proBDNF also increases its binding with p75ntr after seizures that 
      do not cause neuronal death (animals injected with pilocarpine that fail to enter 
      SE). However, in those animals, TrkB protein levels remained unchanged and its 
      phosphorylation increased. Our results indicate an intrinsic capacity of neurons 
      in vivo to modify final neurotrophin output by changing the proportion of their 
      receptors' expression and the receptors' interaction with their ligands. These 
      early events support the idea that neurotrophins may be involved in the induction 
      of neuronal death in vivo under pathological conditions.
FAU - Unsain, N
AU  - Unsain N
AD  - Laboratorio de Neurobiologia, Centro de Biologia Celular y Molecular, Catedra de 
      Biologia Celular, Facultad de Ciencias Exactas, Fisicas y Naturales, Universidad 
      Nacional de Cordoba, Av. Velez Sarsfield 1611, X5016 GCA, Cordoba, Argentina.
FAU - Nunez, N
AU  - Nunez N
FAU - Anastasia, A
AU  - Anastasia A
FAU - Masco, D H
AU  - Masco DH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080502
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Benzoxazines)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Coloring Agents)
RN  - 0 (Fluoresceins)
RN  - 0 (Muscarinic Agonists)
RN  - 0 (Organic Chemicals)
RN  - 0 (Oxazines)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (fluoro jade)
RN  - 01MI4Q9DI3 (Pilocarpine)
RN  - 2AB49C465R (cresyl violet)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Benzoxazines
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Coloring Agents
MH  - Electroshock
MH  - Fluoresceins
MH  - Immunohistochemistry
MH  - Immunoprecipitation
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Muscarinic Agonists
MH  - Neurons/*pathology
MH  - Organic Chemicals
MH  - Oxazines
MH  - Pilocarpine
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Nerve Growth Factor/*metabolism
MH  - Receptor, trkB/*metabolism
MH  - Status Epilepticus/chemically induced/*metabolism/*pathology
EDAT- 2008/05/31 09:00
MHDA- 2008/08/30 09:00
CRDT- 2008/05/31 09:00
PHST- 2007/09/11 00:00 [received]
PHST- 2008/04/03 00:00 [revised]
PHST- 2008/04/04 00:00 [accepted]
PHST- 2008/05/31 09:00 [pubmed]
PHST- 2008/08/30 09:00 [medline]
PHST- 2008/05/31 09:00 [entrez]
AID - S0306-4522(08)00567-8 [pii]
AID - 10.1016/j.neuroscience.2008.04.038 [doi]
PST - ppublish
SO  - Neuroscience. 2008 Jun 26;154(3):978-93. doi: 10.1016/j.neuroscience.2008.04.038. 
      Epub 2008 May 2.