Changes in cytokine expression after electroacupuncture in neuropathic rats.

The production of proinflammatory cytokines including interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) plays a key role in chronic pain such as neuropathic pain. We investigated changes in cytokine expression in injured peripheral nerves and dorsal root ganglia (DRG) following electroacupuncture (EA) treatment. Neuropathic pain was induced by peripheral nerve injury to the left hind limb of Sprague-Dawley rats under pentobarbital anesthesia. Two weeks later, the nerve-injured rats were treated by EA for 10 minutes. The expression levels of IL-1ß, IL-6, and TNF-α in peripheral nerves and DRG of neuropathic rats were significantly increased in nerve-injured rats. However, after EA, the cytokine expression levels were noticeably decreased in peripheral nerves and DRG. These results suggest that EA stimulation can reduce the levels of proinflamtory cytokines elevated after nerve injury.

Modulation of neuropathic pain by galanin and neuropeptide Y at the level of the medulla in rats.

This study was conducted to examine the role of galanin and neuropeptide Y (NPY) in the modulation of neuropathic pain at the level of the medulla. Under pentobarbital anesthesia, Sprague-Dawley rats were subjected to neuropathic surgery. Intracisternal injections of galanin and NPY were performed 2 weeks after nerve injury and mechanical allodynia was monitored. In an electrophysiological experiment, rats were reanesthetized with urethane and the responses of gracile nucleus neurons to mechanical stimulation were observed. Galanin and NPY were applied microiontophoretically. Intracisternally administered NPY reduced neuropathic pain behaviors in a dose-dependent manner. High doses of galanin inhibited neuropathic pain behaviors. Iontophoretically ejected galanin and NPY inhibited responses of gracile nucleus neurons to mechanical stimulation. These results suggest that galanin and NPY play a role in modulating neuropathic pain in the gracile nucleus of the medulla.

Antiallodynic effects of acupuncture in neuropathic rats.

Peripheral nerve injury often results in abnormal neuropathic pain such as allodynia or hyperalgesia. Acupuncture, a traditional Oriental medicine, has been used to relieve pain and related symptoms. However, the efficiency of acupuncture in relieving neuropathic pain is not clear. The aim of this study was to investigate the anti-allodynic effects of acupuncture through behavioral and electrophysiological examinations. Male Sprague-Dawley rats were subjected to neuropathic surgery consisting of a tight ligation and transection of the left tibial and sural nerves, under pentobarbital anesthesia. The acupuncture experiment consisted of four different groups, one treated at each of three different acupoints (Zusanli (ST36), Yinlingquan (SP9), and a sham-acupoint) and a control group. Behavioral tests for mechanical allodynia and cold allodynia were performed for up to two weeks postoperatively. Extracellular electrophysiological recordings were made from the dorsal roots using platinum wire electrodes. Mechanical and cold allodynia were significantly reduced after acupuncture treatment at the Zusanli and Yinlingquan acupoints, respectively. Electrophysiological neural responses to von Frey and acetone tests were also reduced after acupuncture at the same two acupoints. These results suggest that acupuncture may be beneficial in relieving neuropathic pain.

Acute electroacupuncture inhibits nitric oxide synthase expression in the spinal cord of neuropathic rats.

OBJECTIVES: To examine the effects of electroacupuncture stimulation on behavioral changes and neuronal nitric oxide synthase expression in the rat spinal cord after nerve injury. METHODS: Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to neuropathic surgery by tightly ligating and cutting the left tibial and sural nerves. Behavioral responses to mechanical stimulation were tested for 2 weeks post-operatively. At the end of behavioral testing, electroacupuncture stimulation was applied to ST36 (Choksamni) and SP9 (Eumleungcheon) acupoints. Immunocytochemical staining was performed to investigate changes in the expression of neuronal nitric oxide synthase-immunoreactive neurons in the L4-5 spinal cord. RESULTS: Mechanical allodynia was observed by nerve injury. The mechanical allodynia was decreased after electroacupuncture stimulation. Neuronal nitric oxide synthase expression was also decreased in L4-5 spinal cord by electroacupuncture treatment. DISCUSSION: These results suggest that electroacupuncture relieves mechanical allodynia in the neuropathic rats possibly by the inhibition of neuronal nitric oxide synthase expression in the spinal cord.

Modification of cortical excitability in neuropathic rats: a voltage-sensitive dye study.

Recent advances in optical imaging techniques have made it possible to monitor neural activity and provided powerful tools to reveal the spatiotemporal patterns of neural activity. We used optical imaging to determine whether nerve injury affects excitability of the sensory cortex. Male Sprague-Dawley rats were subjected to neuropathic surgery consisting of a tight ligation and transection of the left tibial and sural nerves while under pentobarbital anesthesia. The rats were reanesthetized with urethane two weeks post-operatively, and the exposed cortex surfaces were stained with a voltage-sensitive dye (di-2-ANEPEQ). After electrical stimulation of the receptive field, optical signals from the cerebral cortex were recorded using an optical imaging system. Increased optical intensity and an enlarged area of activation were observed in the cerebral cortex of neuropathic rats during electrical stimulation compared to normal or sham-operated rats. Higher electric stimulation resulted in more intensity and a larger area of activation in neuropathic rats. These results suggest that cortical excitability, resulting from peripheral stimulation, may be affected by nerve injury, which indicates a degree of neural plasticity.