PMID- 24887639
OWN - NLM
STAT- MEDLINE
DCOM- 20150819
LR  - 20220321
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 283
DP  - 2014 Dec 26
TI  - BDNF: no gain without pain?
PG  - 107-23
LID - S0306-4522(14)00444-8 [pii]
LID - 10.1016/j.neuroscience.2014.05.044 [doi]
AB  - Injury to the adult nervous system promotes the expression and secretion of 
      brain-derived neurotrophic factor (BDNF). Because it promotes neuronal growth, 
      survival and neurogenesis, BDNF may initiate compensatory processes that mitigate 
      the deleterious effects of injury, disease or stress. Despite this, BDNF has been 
      implicated in several injury-induced maladaptive processes including pain, 
      spasticity and convulsive activity. This review will concentrate on the 
      predominant role of BDNF in the initiation and maintenance of chronic and/or 
      neuropathic pain at the spinal, peripheral and central levels. Within the spinal 
      dorsal horn, the pattern of BDNF-induced changes in synaptic transmission across 
      five different, identified neuronal phenotypes bears a striking resemblance to 
      that produced by chronic constriction injury (CCI) of peripheral nerves. The 
      appearance of this "pain footprint" thus reflects multiple sensitizing actions of 
      microglial-derived BDNF. These include changes in the chloride equilibrium 
      potential, decreased excitatory synaptic drive to inhibitory neurons, complex 
      changes in inhibitory (GABA/glycinergic) synaptic transmission, increases in 
      excitatory synaptic drive to excitatory neurons and the appearance of oscillatory 
      activity. BDNF effects are confined to changes in synaptic transmission as there 
      is little change in the passive or active properties of neurons in the 
      superficial dorsal horn. Actions of BDNF in the brain stem and periphery also 
      contribute to the onset and persistence of chronic pain. In spite of its role in 
      compensatory processes that facilitate the recovery of the nervous system from 
      injury, the widespread maladaptive actions of BDNF mean that there is literally 
      "no gain without pain".
CI  - Copyright (c) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Smith, Peter A
AU  - Smith PA
AD  - Centre for Neuroscience and Department of Pharmacology, 9.75 Medical Sciences 
      Building, University of Alberta, Edmonton, AB T6G 2H7, Canada. Electronic 
      address: peter.a.smith@ualberta.ca.
LA  - eng
GR  - MOP 81089/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140602
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Humans
MH  - Models, Biological
MH  - Pain/*metabolism/*pathology
MH  - Sensory Receptor Cells/*metabolism
OTO - NOTNLM
OT  - Central sensitization
OT  - dorsal horn
OT  - electrophysiology
OT  - neuropathic pain
OT  - neurotrophin
OT  - organotypic culture
EDAT- 2014/06/03 06:00
MHDA- 2015/08/20 06:00
CRDT- 2014/06/03 06:00
PHST- 2014/03/13 00:00 [received]
PHST- 2014/05/16 00:00 [revised]
PHST- 2014/05/21 00:00 [accepted]
PHST- 2014/06/03 06:00 [entrez]
PHST- 2014/06/03 06:00 [pubmed]
PHST- 2015/08/20 06:00 [medline]
AID - S0306-4522(14)00444-8 [pii]
AID - 10.1016/j.neuroscience.2014.05.044 [doi]
PST - ppublish
SO  - Neuroscience. 2014 Dec 26;283:107-23. doi: 10.1016/j.neuroscience.2014.05.044. 
      Epub 2014 Jun 2.