PMID- 17376001
OWN - NLM
STAT- MEDLINE
DCOM- 20070619
LR  - 20071203
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 24
IP  - 2
DP  - 2007 Feb
TI  - Spinal cord transection enhances afferent-evoked inhibition in lamina II neurons 
      and abolishes BDNF-induced facilitation of their sensory input.
PG  - 379-90
AB  - We previously reported that the pronociceptive neurotrophin brain-derived 
      neurotrophic factor (BDNF) induces facilitation of C-fiber evoked EPSCs and NMDA 
      currents in lamina II neurons of rats up to P40. Here, patch-clamp recording was 
      used to study BDNF-induced modification of synaptic and NMDA-evoked responses in 
      transverse spinal slices from lumbar (L2-L5) spinal cord of rats from P3 to P21 
      following complete spinal cord transection at P2. After transection injury at 
      either T13/L1 or L6/S1, BDNF failed to facilitate synaptic AMPA-kainate currents 
      or agonist-induced NMDA currents. The evoked synaptic currents were smaller in 
      amplitude, often consisting of a biphasic (excitatory-inhibitory) response. The 
      EPSC decayed more rapidly in neurons from transected cords than in those from 
      uninjured cords. In transected cords most neurons responded to the GABA(A) 
      receptor antagonist bicuculline with a significant increase in duration of the 
      excitatory synaptic response. This could subsequently be blocked by D-APV, 
      suggesting an NMDA-receptor mediated component. These findings suggest that 
      following spinal cord transection, BDNF spinal actions are no longer 
      predominantly pronociceptive. It is possible that a diminished availability of 
      full-length TrkB and an enhanced expression of truncated TrkB receptors in the 
      injured cord could play an important role in reducing the effect of BDNF 
      following injury. These data are compared to those obtained after contusion, and 
      it is concluded that the physiological changes after spinal injury differ 
      according to nature of the injury.
FAU - Garraway, Sandra M
AU  - Garraway SM
AD  - Department of Neurobiology and Behavior, State University of New York, Stony 
      Brook, New York 11794, USA.
FAU - Mendell, Lorne M
AU  - Mendell LM
LA  - eng
GR  - P01 NS 39420/NS/NINDS NIH HHS/United States
GR  - R01 NS 16996/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Electric Stimulation
MH  - Lumbar Vertebrae
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/physiology
MH  - Spinal Cord Injuries/complications/*physiopathology
MH  - Substantia Gelatinosa/*physiopathology
MH  - Synaptic Transmission/*physiology
MH  - Thoracic Vertebrae
EDAT- 2007/03/23 09:00
MHDA- 2007/06/20 09:00
CRDT- 2007/03/23 09:00
PHST- 2007/03/23 09:00 [pubmed]
PHST- 2007/06/20 09:00 [medline]
PHST- 2007/03/23 09:00 [entrez]
AID - 10.1089/neu.2006.0115 [doi]
PST - ppublish
SO  - J Neurotrauma. 2007 Feb;24(2):379-90. doi: 10.1089/neu.2006.0115.