PMID- 11731104
OWN - NLM
STAT- MEDLINE
DCOM- 20011217
LR  - 20220330
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 107
IP  - 2
DP  - 2001
TI  - Expression of brain-derived neurotrophic factor in rat dorsal root ganglia, 
      spinal cord and gracile nuclei in experimental models of neuropathic pain.
PG  - 301-9
AB  - Chronic constriction injury of the sciatic nerve and lumbar L5 and L6 spinal 
      nerve ligation provide animal models for pain syndromes accompanying peripheral 
      nerve injury and disease. In the present study, we evaluated changes in 
      brain-derived neurotrophic factor (BDNF) immunoreactivity in the rat L4 and L5 
      dorsal root ganglia (DRG) and areas where afferents from the DRG terminates (the 
      L4/5 spinal cord and gracile nuclei) in these experimental models of neuropathic 
      pain. Chronic constriction injury induced significant increase in the percentage 
      of small, medium and large BDNF-immunoreactive neurons in the ipsilateral L4 and 
      L5 DRG. Following spinal nerve ligation, the percentage of large 
      BDNF-immunoreactive neurons increased significantly, and that of small 
      BDNF-immunoreactive neurons decreased markedly in the ipsilateral L5 DRG, while 
      that of BDNF-immunoreactive L4 DRG neurons of all sizes showed marked increase. 
      Both chronic constriction injury and spinal nerve ligation induced significant 
      increase in the number of BDNF-immunoreactive axonal fibers in the superficial 
      and deeper laminae of the L4/5 dorsal horn and the gracile nuclei on the 
      ipsilateral side. Considering that BDNF may modulate nociceptive sensory inputs 
      and that injection of antiserum to BDNF significantly reduces the sympathetic 
      sprouting in the DRG and allodynic response following sciatic nerve injury, our 
      results also may suggest that endogenous BDNF plays an important role in the 
      induction of neuropathic pain after chronic constriction injury and spinal nerve 
      ligation. In addition, the increase of BDNF in L4 DRG may contribute to evoked 
      pain which is known to be mediated by input from intact afferent from L4 DRG 
      following L5 and L6 spinal nerve ligation.
FAU - Ha, S O
AU  - Ha SO
AD  - Department of Anatomy, School of Medicine, Kyungpook National University, 2-101, 
      Dong-in Dong, Taegu 700-422, South Korea.
FAU - Kim, J K
AU  - Kim JK
FAU - Hong, H S
AU  - Hong HS
FAU - Kim, D S
AU  - Kim DS
FAU - Cho, H J
AU  - Cho HJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
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  - Constriction, Pathologic
MH  - Ganglia, Spinal/*metabolism
MH  - Immunohistochemistry
MH  - Male
MH  - Medulla Oblongata/*metabolism
MH  - Pain/*metabolism
MH  - Peripheral Nervous System Diseases/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sciatic Nerve
MH  - Spinal Cord/*metabolism
MH  - Spinal Nerves
EDAT- 2001/12/04 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/12/04 10:00
PHST- 2001/12/04 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/12/04 10:00 [entrez]
AID - S0306-4522(01)00353-0 [pii]
AID - 10.1016/s0306-4522(01)00353-0 [doi]
PST - ppublish
SO  - Neuroscience. 2001;107(2):301-9. doi: 10.1016/s0306-4522(01)00353-0.