Abstract
BackgroundAdenosine is an endogenous neuromodulator in both the peripheral and central nervous systems. Adenosine inhibits pain signals by hyperpolarizing neuronal membrane. MethodsTo clarify the effects of adenosine on pain signals, we tested intrathecal adenosine injection in two neuropathic pains (spinal cord compression and chronic constriction of sciatic nerve) and postoperative pain (plantar incision). ResultsIn all three kinds of pain models, significant shortening of withdrawal latencies to thermal stimulation were detected from 24h to 1week after the surgery. Significant improvements of pain sensation were observed in all three models after intrathecal injection of Cl-adenosine 24h after surgery. At 72h after surgery, intrathecal Cl-adenosine injection inhibited hyperalgesia in the two neuropathic pain models but not in the postoperative pain model. Adenosine A1R messenger RNA (mRNA) expression significantly decreased in the plantar incision model. Adenosine A1R protein levels also decreased compared with the other two models and normal control. ConclusionsThese results suggest that adenosine effectively inhibits pain signals in neuropathic pain but is less effective in postoperative pain because of the decrease in adenosine A1 receptors.
Highlights
A large number of patients suffer from sciatica, low back, and postoperative pain, treating which is one of the most important topics for clinicians in orthopedic surgery or anesthesiology
To clarify the effects of adenosine on pain signals, we tested intrathecal adenosine injection in two neuropathic pains and postoperative pain
We previously reported that serotonin reuptake inhibitors ameliorated neuropathic pain induced by spinal cord injury [6]
Summary
A large number of patients suffer from sciatica, low back, and postoperative pain, treating which is one of the most important topics for clinicians in orthopedic surgery or anesthesiology. LOR agonists, such as morphine, are commonly used for treating rather serious pain, such as postoperative pain. Monoamines, such as noradrenalin [2] and serotonin [3], are strong endogenous pain-relieving agents. Adenosine is an endogenous neuromodulator that inhibits synaptic transmission in both the peripheral and central nervous systems [7]. The working mechanism of adenosine A1 receptors on pain signals is believed to inhibit pain signals by hyperpolarization of the neuronal membrane. Mice lacking adenosine A1 receptors exhibited increased nociceptive responses [9, 10] These reports indicate that adenosine A1 receptor signal activation may become a new therapeutic method for treating several kinds of pain.
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