PMID- 22613083
OWN - NLM
STAT- MEDLINE
DCOM- 20130114
LR  - 20220207
IS  - 1741-0533 (Electronic)
IS  - 1740-925X (Print)
IS  - 1740-925X (Linking)
VI  - 7
IP  - 1
DP  - 2011 Feb
TI  - Brain-derived neurotrophic factor from microglia: a molecular substrate for 
      neuropathic pain.
PG  - 99-108
LID - 10.1017/S1740925X12000087 [doi]
AB  - One of the most significant advances in pain research is the realization that 
      neurons are not the only cell type involved in the etiology of chronic pain. This 
      realization has caused a radical shift from the previous dogma that neuronal 
      dysfunction alone accounts for pain pathologies to the current framework of 
      thinking that takes into account all cell types within the central nervous system 
      (CNS). This shift in thinking stems from growing evidence that glia can modulate 
      the function and directly shape the cellular architecture of nociceptive networks 
      in the CNS. Microglia, in particular, are increasingly recognized as active 
      principal players that respond to changes in physiological homeostasis by 
      extending their processes toward the site of neural damage, and by releasing 
      specific factors that have profound consequences on neuronal function and that 
      contribute to CNS pathologies caused by disease or injury. A key molecule that 
      modulates microglia activity is ATP, an endogenous ligand of the P2 receptor 
      family. Microglia expresses several P2 receptor subtypes, and of these the P2X4 
      receptor subtype has emerged as a core microglia-neuron signaling pathway: 
      activation of this receptor drives the release of brain-derived neurotrophic 
      factor (BDNF), a cellular substrate that causes disinhibition of 
      pain-transmitting spinal lamina I neurons. Converging evidence points to BDNF 
      from spinal microglia as being a critical microglia-neuron signaling molecule 
      that gates aberrant nociceptive processing in the spinal cord. The present review 
      highlights recent advances in our understanding of P2X4 receptor-mediated 
      signaling and regulation of BDNF in microglia, as well as the implications for 
      microglia-neuron interactions in the pathobiology of neuropathic pain.
FAU - Trang, Tuan
AU  - Trang T
AD  - Program in Neurosciences and Mental Health, Hospital for Sick Children, 
      Department of Physiology, University of Toronto and University of Toronto Centre 
      for Study of Pain, Toronto, Ontario, Canada.
FAU - Beggs, Simon
AU  - Beggs S
FAU - Salter, Michael W
AU  - Salter MW
LA  - eng
GR  - 11219-6/CAPMC/CIHR/Canada
GR  - MT-11219/CAPMC/CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20120522
PL  - England
TA  - Neuron Glia Biol
JT  - Neuron glia biology
JID - 101217278
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cytokines)
RN  - 0 (Receptors, Purinergic P2X)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Central Nervous System/*pathology
MH  - Cytokines/metabolism
MH  - Humans
MH  - Microglia/*metabolism
MH  - Neuralgia/genetics/metabolism/*pathology
MH  - Receptors, Purinergic P2X/metabolism
PMC - PMC3748035
MID - CAMS3159
OID - NLM: CAMS3159
COIS- Statement of Interest: None
EDAT- 2012/05/23 06:00
MHDA- 2013/01/15 06:00
PMCR- 2013/08/20
CRDT- 2012/05/23 06:00
PHST- 2012/05/23 06:00 [entrez]
PHST- 2012/05/23 06:00 [pubmed]
PHST- 2013/01/15 06:00 [medline]
PHST- 2013/08/20 00:00 [pmc-release]
AID - S1740925X12000087 [pii]
AID - 10.1017/S1740925X12000087 [doi]
PST - ppublish
SO  - Neuron Glia Biol. 2011 Feb;7(1):99-108. doi: 10.1017/S1740925X12000087. Epub 2012 
      May 22.