PMID- 28394853
OWN - NLM
STAT- MEDLINE
DCOM- 20180329
LR  - 20240326
IS  - 1872-6623 (Electronic)
IS  - 0304-3959 (Print)
IS  - 0304-3959 (Linking)
VI  - 158
IP  - 7
DP  - 2017 Jul
TI  - Targeting brain-derived neurotrophic factor in the medial thalamus for the 
      treatment of central poststroke pain in a rodent model.
PG  - 1302-1313
LID - 10.1097/j.pain.0000000000000915 [doi]
AB  - Approximately 7% to 10% of patients develop a chronic pain syndrome after stroke. 
      This chronic pain condition is called central poststroke pain (CPSP). Recent 
      studies have observed an abnormal increase in the secretion of brain-derived 
      neurotrophic factor (BDNF) in spinal cord tissue after spinal cord injury. An 
      animal model of CPSP was established by an intrathalamus injection of 
      collagenase. Mechanical and thermal allodynia was induced after lesions of the 
      thalamic ventral basal complex in rats. Four weeks after the injection, the 
      number of neurons decreased, the number of astrocytes, microglia, and P2X4 
      receptors increased, and BDNF mRNA expression increased in the brain lesion area. 
      Nociceptive activity in the medial thalamus (MT) and the coherence coefficient of 
      spontaneous field potential oscillations in the anterior cingulate cortex were 
      enhanced in CPSP animals, and these enhancements were blocked by an acute 
      injection of TrkB-Fc and TrkB antagonist Tat Cyclotraxin-B. Instead of being 
      inhibited by the gamma-aminobutyric acid (GABA) system in normal rats, multiunit 
      activity in the MT was enhanced after a microinjection of muscimol, a GABAA 
      receptor agonist, in CPSP animals. After CPSP, BDNF expression was enhanced in 
      the MT, whereas the expression of GABAA channels and the cotransporter KCC2 
      decreased in the same area. These findings suggest that neuronal plasticity in 
      the MT that was induced by BDNF overexpression after the thalamic lesion was a 
      key factor in CPSP.
FAU - Shih, Hsi-Chien
AU  - Shih HC
AD  - Neuroscience, Institute of Biomedical Science, Academia Sinica, Taipei, Taiwan.
FAU - Kuan, Yung-Hui
AU  - Kuan YH
FAU - Shyu, Bai-Chung
AU  - Shyu BC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Pain
JT  - Pain
JID - 7508686
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (GABA-A Receptor Agonists)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (cyclotraxin-B)
RN  - 2763-96-4 (Muscimol)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Disease Models, Animal
MH  - GABA-A Receptor Agonists/pharmacology
MH  - Male
MH  - Mediodorsal Thalamic Nucleus/drug effects/*metabolism
MH  - Muscimol/pharmacology
MH  - Neuronal Plasticity/drug effects
MH  - Neurons/drug effects/metabolism
MH  - Pain/*drug therapy/etiology/metabolism
MH  - Pain Management/*methods
MH  - Peptides, Cyclic/pharmacology/*therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/*antagonists & inhibitors
MH  - Stroke/complications/*metabolism
PMC - PMC5472007
EDAT- 2017/04/11 06:00
MHDA- 2018/03/30 06:00
PMCR- 2017/06/15
CRDT- 2017/04/11 06:00
PHST- 2017/04/11 06:00 [pubmed]
PHST- 2018/03/30 06:00 [medline]
PHST- 2017/04/11 06:00 [entrez]
PHST- 2017/06/15 00:00 [pmc-release]
AID - 00006396-201707000-00016 [pii]
AID - PAIN-D-17-00038 [pii]
AID - 10.1097/j.pain.0000000000000915 [doi]
PST - ppublish
SO  - Pain. 2017 Jul;158(7):1302-1313. doi: 10.1097/j.pain.0000000000000915.