Abstract
BackgroundRecent 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.MethodsThe 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).ResultsThe 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.ConclusionsThe 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.
Highlights
Recent evidence suggests that persistent pain and recurrent pain are due to the pain memory which is related to the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (p-cAMP response elementbinding protein (CREB)) in anterior cingulate cortex (ACC)
Following the model establishment and testing of mechanical allodynia (Figure 1), we investigated the changes in paw withdrawal thresholds (PWTs) after two carrageenan injections separated by a 14-day interval
Fourteen days after the pain withdrawal thresholds had returned to its baseline, the second injection of carrageenan to the previously non-injected hind paw caused a similar decrease of PWTs in the left hind paw from 4 h to 72 h
Summary
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). Patients who suffer from nociceptive pain for a long time may feel persistent pain even after recovery of the initial cause of pain [1,2]. Sun et al Behavioral and Brain Functions (2015) 11:9 inhibit the memory of pain become an effective way of analgesia for prolonged pain. Evidence suggests that the anterior cingulate cortex (ACC), the insular cortex, and the amygdala are examples of regions implicated in both pain and memory [4]. Based on functional magnetic resonance imaging (fMRI) studies in both rats and humans, the ACC is involved in pain memory processing [7,8]
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