PMID- 22496528
OWN - NLM
STAT- MEDLINE
DCOM- 20121212
LR  - 20120716
IS  - 1522-1598 (Electronic)
IS  - 0022-3077 (Linking)
VI  - 108
IP  - 2
DP  - 2012 Jul
TI  - Long-term actions of BDNF on inhibitory synaptic transmission in identified 
      neurons of the rat substantia gelatinosa.
PG  - 441-52
LID - 10.1152/jn.00457.2011 [doi]
AB  - Peripheral nerve injury promotes the release of brain-derived neurotrophic factor 
      (BDNF) from spinal microglial cells and primary afferent terminals. This induces 
      an increase in dorsal horn excitability that contributes to "central 
      sensitization" and to the onset of neuropathic pain. Although it is accepted that 
      impairment of GABAergic and/or glycinergic inhibition contributes to this 
      process, certain lines of evidence suggest that GABA release in the dorsal horn 
      may increase after nerve injury. To resolve these contradictory findings, we 
      exposed rat spinal cord neurons in defined-medium organotypic culture to 200 
      ng/ml BDNF for 6 days to mimic the change in spinal BDNF levels that accompanies 
      peripheral nerve injury. Morphological and electrophysiological criteria and 
      glutamic acid decarboxylase (GAD) immunohistochemistry were used to distinguish 
      putative inhibitory tonic-islet-central neurons from putative excitatory 
      delay-radial neurons. Whole cell recording in the presence of 1 muM tetrodotoxin 
      showed that BDNF increased the amplitude of GABAergic and glycinergic miniature 
      inhibitory postsynaptic currents (mIPSCs) in both cell types. It also increased 
      the amplitude and frequency of spontaneous, action potential-dependent IPSCs 
      (sIPSCs) in putative excitatory neurons. By contrast, BDNF reduced sIPSC 
      amplitude in inhibitory neurons but frequency was unchanged. This increase in 
      inhibitory drive to excitatory neurons and decreased inhibitory drive to 
      inhibitory neurons seems inconsistent with the observation that BDNF increases 
      overall dorsal horn excitability. One of several explanations for this 
      discrepancy is that the action of BDNF in the substantia gelatinosa is dominated 
      by previously documented increases in excitatory synaptic transmission rather 
      than by impediment of inhibitory transmission.
FAU - Lu, Van B
AU  - Lu VB
AD  - Department of Pharmacology and Centre for Neuroscience, University of Alberta, 
      Edmonton, Alberta, Canada.
FAU - Colmers, William F
AU  - Colmers WF
FAU - Smith, Peter A
AU  - Smith PA
LA  - eng
GR  - 81089/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120411
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Action Potentials/drug effects/*physiology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Long-Term Potentiation/drug effects/*physiology
MH  - Neural Inhibition/drug effects/*physiology
MH  - Neurons/drug effects/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Substantia Gelatinosa/drug effects/*physiology
MH  - Synaptic Transmission/drug effects/*physiology
EDAT- 2012/04/13 06:00
MHDA- 2012/12/13 06:00
CRDT- 2012/04/13 06:00
PHST- 2012/04/13 06:00 [entrez]
PHST- 2012/04/13 06:00 [pubmed]
PHST- 2012/12/13 06:00 [medline]
AID - jn.00457.2011 [pii]
AID - 10.1152/jn.00457.2011 [doi]
PST - ppublish
SO  - J Neurophysiol. 2012 Jul;108(2):441-52. doi: 10.1152/jn.00457.2011. Epub 2012 Apr 
      11.