PMID- 18158214
OWN - NLM
STAT- MEDLINE
DCOM- 20081006
LR  - 20210112
IS  - 1872-6623 (Electronic)
IS  - 0304-3959 (Linking)
VI  - 138
IP  - 1
DP  - 2008 Aug 15
TI  - Spinal brain-derived neurotrophic factor governs neuroplasticity and recovery 
      from cold-hypersensitivity following dorsal rhizotomy.
PG  - 98-110
LID - 10.1016/j.pain.2007.11.014 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) has multiple effects on 
      tropomyosin-related receptor kinase B--(TrkB) expressing neurons, including 
      potentiation of spinal nociceptive transmission and stimulation of axon 
      outgrowth. BDNF is upregulated in the spinal cord following dorsal root injury 
      (DRI), a manipulation which elicits both pain and collateral sprouting. 
      Transection of the C7 and C8 dorsal roots (C7/8 DRI) generates cold pain in the 
      ipsilateral forepaw which peaks at 10 days, and resolves within three weeks after 
      injury. In the present study, we investigated the influence of chronic BDNF 
      sequestration, by intrathecal delivery of TrkB-Fc, on the plasticity of 
      nociceptive circuitry and resultant cold pain behaviour following spinal 
      deafferentation. C7/8 DRI resulted in a pronounced deafferentation of the C7 
      dorsal horn and significant depletion of both peptidergic- and non-peptidergic 
      nociceptive projections. While changes in GAP-43 expression revealed that 
      endogenous BDNF was exerting an overall plasticity-promoting influence on 
      intraspinal axons after DRI, continuous TrkB-Fc treatment stimulated sprouting of 
      nociceptive terminals. DRI stimulated a BDNF-dependent increase in the density of 
      GABAergic interneuronal processes, as indicated by increased vesicular GABA 
      transporter--(VGAT) and neuropeptide Y--(NPY) positive terminal densities. 
      Finally, chronic TrkB-Fc treatment prevented cold pain resolution. These findings 
      demonstrate that endogenous BDNF has both plasticity-promoting and 
      plasticity-suppressing effects on the intrinsic spinal components of nociceptive 
      circuitry, which are likely to underlie cold pain behaviour following C7/8 DRI.
FAU - Soril, Lesley J J
AU  - Soril LJJ
AD  - ICORD (International Collaboration on Repair Discoveries), The University of 
      British Columbia, Room 2469, Biosciences Building, 6270 University Boulevard, 
      Vancouver, BC, Canada V6T 1Z4 Neurorestoration Group, Wolfson Centre for 
      Age-Related Diseases, Wolfson Wing, Hodgkin Building, King's College London, 
      Guy's Campus, London Bridge, London SE1 1UL, UK.
FAU - Ramer, Leanne M
AU  - Ramer LM
FAU - McPhail, Lowell T
AU  - McPhail LT
FAU - Kaan, Timothy K Y
AU  - Kaan TKY
FAU - Ramer, Matt S
AU  - Ramer MS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071226
PL  - United States
TA  - Pain
JT  - Pain
JID - 7508686
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cold Temperature
MH  - Ganglia, Spinal/*physiopathology/*surgery
MH  - Hyperalgesia/*physiopathology
MH  - Male
MH  - *Neuronal Plasticity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Recovery of Function
MH  - *Rhizotomy
EDAT- 2007/12/26 09:00
MHDA- 2008/10/07 09:00
CRDT- 2007/12/26 09:00
PHST- 2007/10/09 00:00 [received]
PHST- 2007/11/07 00:00 [revised]
PHST- 2007/11/19 00:00 [accepted]
PHST- 2007/12/26 09:00 [pubmed]
PHST- 2008/10/07 09:00 [medline]
PHST- 2007/12/26 09:00 [entrez]
AID - 00006396-200808150-00014 [pii]
AID - 10.1016/j.pain.2007.11.014 [doi]
PST - ppublish
SO  - Pain. 2008 Aug 15;138(1):98-110. doi: 10.1016/j.pain.2007.11.014. Epub 2007 Dec 
      26.