PMID- 21864655
OWN - NLM
STAT- MEDLINE
DCOM- 20120405
LR  - 20111115
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Linking)
VI  - 86
IP  - 5-6
DP  - 2011 Nov 25
TI  - Involvement of spinal cord BDNF in the generation and maintenance of chronic 
      neuropathic pain in rats.
PG  - 454-9
LID - 10.1016/j.brainresbull.2011.08.008 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) is involved in neuronal survival and 
      synaptic plasticity of the central and peripheral nervous system. In chronic 
      pain, plastic changes in dorsal horn neurons contribute to a phenomenon of 
      hypersensitivity to pain sensation that is maintained over time, known as central 
      sensitization. This process is accompanied by BDNF overexpression, but the role 
      of BDNF in the generation and maintenance of the hyperalgesic phenomenon is still 
      unclear. The present study was aimed to investigate if exogenous BDNF 
      administered to the rat spinal cord, in addition to trigger pain, participates in 
      the maintenance of the central sensitization process (i.e., pain persistence) and 
      to determine if the pain generated is comparable to that observed in a 
      neuropathic pain model. Results showed that a single intrathecal injection of 
      0.003 ng of BDNF was able to decrease the nociceptive threshold (Randall-Selitto 
      test) in normal rats, for at least a 42-day period. Furthermore, the hyperalgesia 
      generated was comparable to that observed in rats with a 42-day history of 
      mononeuropathy. Increasing the dose or administering additional doses of BDNF 
      resulted neither in additional effectiveness in reducing the pain threshold nor 
      in the prolongation of the hyperalgesic effect, thus showing that central 
      sensitization induced by BDNF is a dose-independent, all-or-none process. It is 
      concluded that BDNF alone is sufficient for generating a long-lasting neural 
      excitability change in the spinal cord via tyrosine kinase B receptor signaling, 
      similar to that observed in chronic pain models such as neuropathy.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Constandil, Luis
AU  - Constandil L
AD  - Laboratorio de Neurobiologia, Departamento de Biologia, Facultad de Quimica y 
      Biologia, Universidad de Santiago de Chile, Santiago, Chile.
FAU - Aguilera, Rodrigo
AU  - Aguilera R
FAU - Goich, Mariela
AU  - Goich M
FAU - Hernandez, Alejandro
AU  - Hernandez A
FAU - Alvarez, Pedro
AU  - Alvarez P
FAU - Infante, Claudio
AU  - Infante C
FAU - Pelissier, Teresa
AU  - Pelissier T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110816
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Central Nervous System Sensitization/*drug effects
MH  - Humans
MH  - Injections, Spinal
MH  - Male
MH  - Neuralgia/*chemically induced/*physiopathology
MH  - Pain Measurement
MH  - Pain Threshold/*drug effects
MH  - Posterior Horn Cells/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/metabolism
MH  - Spinal Cord/cytology/*drug effects
EDAT- 2011/08/26 06:00
MHDA- 2012/04/06 06:00
CRDT- 2011/08/26 06:00
PHST- 2011/05/20 00:00 [received]
PHST- 2011/08/08 00:00 [revised]
PHST- 2011/08/09 00:00 [accepted]
PHST- 2011/08/26 06:00 [entrez]
PHST- 2011/08/26 06:00 [pubmed]
PHST- 2012/04/06 06:00 [medline]
AID - S0361-9230(11)00255-3 [pii]
AID - 10.1016/j.brainresbull.2011.08.008 [doi]
PST - ppublish
SO  - Brain Res Bull. 2011 Nov 25;86(5-6):454-9. doi: 
      10.1016/j.brainresbull.2011.08.008. Epub 2011 Aug 16.