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Electroacupuncture alleviates retrieval of pain memory and its effect on phosphorylation of cAMP response element-binding protein in anterior cingulate cortex in rats.

Sun J, Shao XM, Fang F, Shen Z, Wu YY, Fang JQ - Behav Brain Funct (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, China. sunjing0268@163.com.

ABSTRACT

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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Co-localization of p-CREB and GFAP in coronal brain sections of ACC. Photomicrographs showed the expression of p-CREB (red) and GFAP (an astrocytic marker, green) from the same sections in figure a. Figure b was a high magnification image of the areas indicated by the yellow squares in the figure a. The double-immunofluorescence labeling showed that p-CREB co-expressed with GFAP in the ACC. Numbers of GFAP-positive cells and co-localization of p-CREB with GFAP were analysed in figure c and d. Error bars indicated standard error of the mean. Four rats for each group, five slides for each rat. * p < 0.05, ** p < 0.01 vs. the control group; ## p < 0.01 vs. the model group.
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Fig4: Co-localization of p-CREB and GFAP in coronal brain sections of ACC. Photomicrographs showed the expression of p-CREB (red) and GFAP (an astrocytic marker, green) from the same sections in figure a. Figure b was a high magnification image of the areas indicated by the yellow squares in the figure a. The double-immunofluorescence labeling showed that p-CREB co-expressed with GFAP in the ACC. Numbers of GFAP-positive cells and co-localization of p-CREB with GFAP were analysed in figure c and d. Error bars indicated standard error of the mean. Four rats for each group, five slides for each rat. * p < 0.05, ** p < 0.01 vs. the control group; ## p < 0.01 vs. the model group.

Mentions: The results from IF showed a substantial increase in the number of GFAP-positive cells after retrieval of pain memory, compared with that in the control group (P < 0.05). EA treatment produced no obvious decrease of GFAP-positive cells in ACC compared with the model group (Figure 4a, c). The double immunofluorescence examinations showed remarkably increased numbers of GFAP-positive cells co-expressing p-CREB in the model group, compared with those in the control group (P < 0.01). In contrast to the lack of changes in GFAP immunostaining after EA intervention, the decreased numbers of GFAP-positive cells co-expressing p-CREB were observed, compared to those in the model group (P < 0.01) (Figure 4b, d).Figure 4


Electroacupuncture alleviates retrieval of pain memory and its effect on phosphorylation of cAMP response element-binding protein in anterior cingulate cortex in rats.

Sun J, Shao XM, Fang F, Shen Z, Wu YY, Fang JQ - Behav Brain Funct (2015)

Co-localization of p-CREB and GFAP in coronal brain sections of ACC. Photomicrographs showed the expression of p-CREB (red) and GFAP (an astrocytic marker, green) from the same sections in figure a. Figure b was a high magnification image of the areas indicated by the yellow squares in the figure a. The double-immunofluorescence labeling showed that p-CREB co-expressed with GFAP in the ACC. Numbers of GFAP-positive cells and co-localization of p-CREB with GFAP were analysed in figure c and d. Error bars indicated standard error of the mean. Four rats for each group, five slides for each rat. * p < 0.05, ** p < 0.01 vs. the control group; ## p < 0.01 vs. the model group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4364627&req=5

Fig4: Co-localization of p-CREB and GFAP in coronal brain sections of ACC. Photomicrographs showed the expression of p-CREB (red) and GFAP (an astrocytic marker, green) from the same sections in figure a. Figure b was a high magnification image of the areas indicated by the yellow squares in the figure a. The double-immunofluorescence labeling showed that p-CREB co-expressed with GFAP in the ACC. Numbers of GFAP-positive cells and co-localization of p-CREB with GFAP were analysed in figure c and d. Error bars indicated standard error of the mean. Four rats for each group, five slides for each rat. * p < 0.05, ** p < 0.01 vs. the control group; ## p < 0.01 vs. the model group.
Mentions: The results from IF showed a substantial increase in the number of GFAP-positive cells after retrieval of pain memory, compared with that in the control group (P < 0.05). EA treatment produced no obvious decrease of GFAP-positive cells in ACC compared with the model group (Figure 4a, c). The double immunofluorescence examinations showed remarkably increased numbers of GFAP-positive cells co-expressing p-CREB in the model group, compared with those in the control group (P < 0.01). In contrast to the lack of changes in GFAP immunostaining after EA intervention, the decreased numbers of GFAP-positive cells co-expressing p-CREB were observed, compared to those in the model group (P < 0.01) (Figure 4b, d).Figure 4

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, China. sunjing0268@163.com.

ABSTRACT

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.

Show MeSH