Electroacupuncture alleviates retrieval of pain memory and its effect on phosphorylation of cAMP response element-binding protein in anterior cingulate cortex in rats
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  • 作者:Jing Sun (1)
    Xiao-mei Shao (1)
    Fang Fang (1)
    Zui Shen (1)
    Yuan-yuan Wu (1)
    Jian-qiao Fang (1)

    1. Department of Neurobiology and Acupuncture Research
    ; The Third Clinical Medical College ; Zhejiang Chinese Medical University ; Hangzhou ; China
  • 关键词:Electroacupuncture ; Pain memory ; Phosphorylation of cAMP response elment ; binding protein ; Anterior cingulate cortex ; Rat
  • 刊名:Behavioral and Brain Functions
  • 出版年:2015
  • 出版时间:December 2015
  • 年:2015
  • 卷:11
  • 期:1
  • 全文大小:3,829 KB
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  • 刊物主题:Neurosciences; Neurology; Behavioral Therapy;
  • 出版者:BioMed Central
  • ISSN:1744-9081
文摘
Background Recent evidence suggests that persistent pain and recurrent pain are due to the pain memory which is related to the phosphorylation of cAMP response element-binding protein (p-CREB) in anterior cingulate cortex (ACC). Eletroacupuncture (EA), as a complementary Chinese medical procedure, has a significant impact on the treatment of pain and is now considered as a mind-body therapy. Methods The rat model of pain memory was induced by two injections of carrageenan into the paws, which was administered separately by a 14-day interval, and treated with EA therapy. The paw withdrawal thresholds (PWTs) of animals were measured and p-CREB expressions in ACC were detected by using immunofluorescence (IF) and electrophoretic mobility shift assay (EMSA). Statistical comparisons among different groups were made by one-way, repeated-measures analysis of variance (ANOVA). Results The second injection of carrageenan caused the decrease of PWTs in the non-injected hind paw. EA stimulation applied prior to the second injection, increased the values of PWTs. In ACC, the numbers of p-CREB positive cells were significantly increased in pain memory model rats, which were significantly reduced by EA. EMSA results showed EA also down-regulated the combining capacity of p-CREB with its DNA. Furthermore, the co-expression of p-CREB with GFAP, OX-42, or NeuN in ACC was strengthened in the pain memory model rats. EA inhibited the co-expression of p-CREB with GFAP or OX-42, but not NeuN in ACC. Conclusions The present results suggest the retrieval of pain memory could be alleviated by the pre-treatment of EA, which is at least partially attributed to the down-regulated expression and combining capacity of p-CREB and the decreased expression of p-CREB in astrocytes and microglia cells.

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