PMID- 25355226
OWN - NLM
STAT- MEDLINE
DCOM- 20150106
LR  - 20211021
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 34
IP  - 44
DP  - 2014 Oct 29
TI  - BDNF-dependent plasticity induced by peripheral inflammation in the primary 
      sensory and the cingulate cortex triggers cold allodynia and reveals a major role 
      for endogenous BDNF as a tuner of the affective aspect of pain.
PG  - 14739-51
LID - 10.1523/JNEUROSCI.0860-14.2014 [doi]
AB  - Painful experiences are multilayered, composed of sensory, affective, cognitive 
      and behavioral facets. Whereas it is well accepted that the development of 
      chronic pain is due to maladaptive neuronal changes, the underlying molecular 
      mechanisms, their relationship to the different pain modalities, and indeed the 
      localization of these changes are still unknown. Brain-derived neurotrophic 
      factor (BDNF) is an activity-dependent neuromodulator in the adult brain, which 
      enhances neuronal excitability. In the spinal cord, BDNF underlies the 
      development and maintenance of inflammatory and neuropathic pain. Here, we 
      hypothesized that BDNF could be a trigger of some of these plastic changes. Our 
      results demonstrate that BDNF is upregulated in the anterior cingulate cortex 
      (ACC) and the primary sensory cortex (S1) in rats with inflammatory pain. 
      Injections of recombinant BDNF (into the ACC) or a viral vector synthesizing BDNF 
      (into the ACC or S1) triggered both neuronal hyperexcitability, as shown by 
      elevated long-term potentiation, and sustained pain hypersensitivity. Finally, 
      pharmacological blockade of BDNF-tropomyosin receptor kinase B (TrkB) signaling 
      in the ACC, through local injection of cyclotraxin-B (a novel, highly potent, and 
      selective TrkB antagonist) prevented neuronal hyperexcitability, the emergence of 
      cold hypersensitivity, and passive avoidance behavior. These findings show that 
      BDNF-dependent neuronal plasticity in the ACC, a structure known to be involved 
      in the affective-emotional aspect of pain, is a key mechanism in the development 
      and maintenance of the emotional aspect of chronic pain.
CI  - Copyright (c) 2014 the authors 0270-6474/14/3414739-13$15.00/0.
FAU - Thibault, Karine
AU  - Thibault K
AD  - Brain Plasticity Unit, ESPCI-ParisTech, 75005 Paris, France, Centre National de 
      la Recherche Scientifique, UMR 8249, 75794 Paris cedex 16, France.
FAU - Lin, Wee Khang
AU  - Lin WK
AD  - Department of Pharmacology, University of Oxford, Oxford OX1 3QT, United Kingdom.
FAU - Rancillac, Armelle
AU  - Rancillac A
AD  - Brain Plasticity Unit, ESPCI-ParisTech, 75005 Paris, France, Centre National de 
      la Recherche Scientifique, UMR 8249, 75794 Paris cedex 16, France.
FAU - Fan, Marie
AU  - Fan M
AD  - Brain Plasticity Unit, ESPCI-ParisTech, 75005 Paris, France, Centre National de 
      la Recherche Scientifique, UMR 8249, 75794 Paris cedex 16, France.
FAU - Snollaerts, Thibaut
AU  - Snollaerts T
AD  - Organisation Nucleaire et Oncogenese, INSERM U993, Departement de Biologie 
      Cellulaire et Infection, Institut Pasteur, 75015 Paris, France.
FAU - Sordoillet, Vallier
AU  - Sordoillet V
AD  - Brain Plasticity Unit, ESPCI-ParisTech, 75005 Paris, France, Centre National de 
      la Recherche Scientifique, UMR 8249, 75794 Paris cedex 16, France.
FAU - Hamon, Michel
AU  - Hamon M
AD  - UMR894 INSERM-CPN-UPMC, Faculte de Medecine Pierre et Marie Curie, Site 
      Pitie-Salpetriere, 75634 Paris cedex 13, France, and.
FAU - Smith, George M
AU  - Smith GM
AD  - Shriners Hospitals Pediatric Research Center, Temple University, School of 
      Medicine, Philadelphia, Pennsylvania 19140-5104.
FAU - Lenkei, Zsolt
AU  - Lenkei Z
AD  - Brain Plasticity Unit, ESPCI-ParisTech, 75005 Paris, France, Centre National de 
      la Recherche Scientifique, UMR 8249, 75794 Paris cedex 16, France.
FAU - Pezet, Sophie
AU  - Pezet S
AD  - Brain Plasticity Unit, ESPCI-ParisTech, 75005 Paris, France, Centre National de 
      la Recherche Scientifique, UMR 8249, 75794 Paris cedex 16, France, 
      sophie.pezet@espci.fr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (cyclotraxin-B)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Affect/drug effects/*physiology
MH  - Animals
MH  - Behavior, Animal/drug effects/physiology
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism/pharmacology
MH  - Gyrus Cinguli/drug effects/*metabolism/physiopathology
MH  - Hyperalgesia/chemically induced/*metabolism/physiopathology
MH  - Inflammation/chemically induced/metabolism/physiopathology
MH  - Male
MH  - Neuronal Plasticity/drug effects/*physiology
MH  - Peptides, Cyclic/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/antagonists & inhibitors
MH  - Somatosensory Cortex/drug effects/*metabolism/physiopathology
MH  - Up-Regulation/physiology
PMC - PMC6608422
OTO - NOTNLM
OT  - hyperexcitability
OT  - neurotrophic factor
OT  - pain
OT  - viral vector
EDAT- 2014/10/31 06:00
MHDA- 2015/01/07 06:00
PMCR- 2015/04/29
CRDT- 2014/10/31 06:00
PHST- 2014/10/31 06:00 [entrez]
PHST- 2014/10/31 06:00 [pubmed]
PHST- 2015/01/07 06:00 [medline]
PHST- 2015/04/29 00:00 [pmc-release]
AID - 34/44/14739 [pii]
AID - 0860-14 [pii]
AID - 10.1523/JNEUROSCI.0860-14.2014 [doi]
PST - ppublish
SO  - J Neurosci. 2014 Oct 29;34(44):14739-51. doi: 10.1523/JNEUROSCI.0860-14.2014.