Abstract
This study examined the influence of the N-methyl-D-aspartate receptor (NMDAR) on the modulation of related spinal signaling after electroacupuncture (EA) treatment in normal rats. Bilateral 2 Hz EA stimulations (1-2-3.0 mA) were delivered at acupoints corresponding to Zusanli (ST36) and Sanyinjiao (SP6) in men for 30 min. Thermal sensitization was strongly inhibited by EA, but this analgesia was reduced by preintrathecal injection of the NMDAR antagonist, MK801. Phosphorylation of the NMDAR NR2B subunit, cAMP response element-binding protein (CREB), and especially phosphatidylinositol 3-kinase (PI3K) were significantly induced by EA. However, these marked phosphorylations were not observed in MK801-pretreated rats. EA analgesia was reduced by preintrathecal injection with the calcium chelators Quin2 and TMB8, similar to the results evident using MK801. Phosphorylation of PI3K and CREB induced by EA was also inhibited by TMB8. Calcium influx by NMDAR activation may play an important role in EA analgesia of normal rats through the modulation of the phosphorylation of spinal PI3K and CREB.
Highlights
Electroacupuncture (EA), a new and modern type of traditional acupuncture, is widely used to treat various types of diseases in a clinical setting with the alterations of peripheral electrical stimulation rather than hand manipulation [1]
The NR2B subunit has an important function in spinal dorsal horn sensory pathways, and phosphorylation of this subunit plays a role in the induction of long-term potentiation (LTP), a phenomenon related to central sensitization [7, 8]
EA stimulation markedly reduces inflammatory hyperalgesia by inhibiting the release of glutamate in the spinal dorsal horn, and N-methyl-D-aspartate receptor (NMDAR) antagonists display an antinociceptive action in an inflammatory pain model [19]
Summary
Electroacupuncture (EA), a new and modern type of traditional acupuncture, is widely used to treat various types of diseases in a clinical setting with the alterations of peripheral electrical stimulation rather than hand manipulation [1]. The activation of NMDAR plays an important role in the induction and maintenance of hyperalgesia in the spinal dorsal horn [4,5,6]. The NR2B subunit has an important function in spinal dorsal horn sensory pathways, and phosphorylation of this subunit plays a role in the induction of long-term potentiation (LTP), a phenomenon related to central sensitization [7, 8]. NMDAR containing the NR2B subunit localizes in the extrasynaptic membrane [9] Their activations are involved in a variety of pain states including the development of central sensitization via the induction of LTP in the dorsal horn of the spinal cord [10, 11]
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