PMID- 22854425
OWN - NLM
STAT- MEDLINE
DCOM- 20130306
LR  - 20210112
IS  - 1872-6623 (Electronic)
IS  - 0304-3959 (Linking)
VI  - 153
IP  - 10
DP  - 2012 Oct
TI  - Impairment of long-term depression in the anterior cingulate cortex of mice with 
      bone cancer pain.
PG  - 2097-2108
LID - 10.1016/j.pain.2012.06.031 [doi]
AB  - The anterior cingulate cortex (ACC) has been shown to play an important role in 
      pain-related perception and chronic pain. However, little is known about the 
      molecular mechanisms involved. To address this issue, we analyzed excitatory 
      synaptic transmission and long-term synaptic plasticity in layer II/III pyramidal 
      neurons within the rostral ACC (rACC) from mice with bone cancer pain induced by 
      intra-tibia implantation of osteolytic fibrosarcoma cells. Ex vivo whole-cell 
      patch-clamp recordings from rACC neurons showed no significant alterations in 
      presynaptic glutamate release probability and postsynaptic 
      alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated 
      synaptic responses in mice with bone cancer pain. However, mechanical allodynia 
      occurred in conjunction with decreased N-methyl-d-aspartate (NMDA)/AMPA ratio of 
      synaptic currents elicited in bilateral rACC neurons. In addition, the induction 
      of NMDA receptor-dependent long-term depression (LTD) at rACC synapses was 
      impaired in rACC neurons of tumor-bearing mice. Western blot analysis revealed a 
      significant decrease in the levels of NR1, NR2A, and NR2B subunits of NMDA 
      receptors in the rACC under bone cancer pain condition. No significant changes in 
      overall mRNA levels for any of the NMDA receptor subunits or calpain activity 
      were observed in the rACC of tumor-bearing mice. These results indicate that 
      tumor-induced injury or remodeling of primary afferent sensory nerve fibers that 
      innervate the tumor-bearing bone may cause a persistent decrease in NMDA receptor 
      expression in rACC neurons, resulting in a loss of LTD induction, thereby leading 
      to long-term alterations of rACC activity and creating exaggerated pain 
      behaviors.
CI  - Copyright (c) 2012 International Association for the Study of Pain. Published by 
      Elsevier B.V. All rights reserved.
FAU - Chiou, Chiuan-Shiou
AU  - Chiou CS
AD  - Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung 
      University, Tainan 701, Taiwan Department of Anesthesiology, National Cheng Kung 
      University Hospital, Tainan 704, Taiwan Department of Pharmacology, College of 
      Medicine, National Cheng Kung University, Tainan 701, Taiwan.
FAU - Huang, Chiung-Chun
AU  - Huang CC
FAU - Liang, Ying-Ching
AU  - Liang YC
FAU - Tsai, Yu-Chuan
AU  - Tsai YC
FAU - Hsu, Kuei-Sen
AU  - Hsu KS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120731
PL  - United States
TA  - Pain
JT  - Pain
JID - 7508686
SB  - IM
MH  - Animals
MH  - Bone Neoplasms/*complications/*physiopathology
MH  - Gyrus Cinguli/*physiopathology
MH  - *Long-Term Synaptic Depression
MH  - Male
MH  - Mice
MH  - Mice, Inbred C3H
MH  - *Neural Inhibition
MH  - Neuronal Plasticity
MH  - Pain/*etiology/*physiopathology
EDAT- 2012/08/03 06:00
MHDA- 2013/03/07 06:00
CRDT- 2012/08/03 06:00
PHST- 2012/03/09 00:00 [received]
PHST- 2012/06/23 00:00 [revised]
PHST- 2012/06/29 00:00 [accepted]
PHST- 2012/08/03 06:00 [entrez]
PHST- 2012/08/03 06:00 [pubmed]
PHST- 2013/03/07 06:00 [medline]
AID - 00006396-201210000-00019 [pii]
AID - 10.1016/j.pain.2012.06.031 [doi]
PST - ppublish
SO  - Pain. 2012 Oct;153(10):2097-2108. doi: 10.1016/j.pain.2012.06.031. Epub 2012 Jul 
      31.