scholarly journals Regulation of Neurotrophin-3 and Interleukin-1βand Inhibition of Spinal Glial Activation Contribute to the Analgesic Effect of Electroacupuncture in Chronic Neuropathic Pain States of Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Wenzhan Tu ◽  
Wansheng Wang ◽  
Haiyan Xi ◽  
Rong He ◽  
Liping Gao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Analgesic Effect ◽  
Dorsal Root ◽  
Interleukin 1 ◽  
Chronic Neuropathic Pain ◽  
Western Blots ◽  
Withdrawal Threshold ◽  
Withdrawal Latency ◽  
Neurotrophin 3

Growing evidence indicates that neurotrophin-3, interleukin-1β, and spinal glia are involved in neuropathic pain derived from dorsal root ganglia to spinal cord. Electroacupuncture is widely accepted to treat chronic pain, but the precise mechanism underlying the analgesic effect of EA has not been fully demonstrated. In this study, the mechanical withdrawal threshold and thermal withdrawal latency were recorded. We used immunofluorescence and western blots methods to investigate the effect of EA on the expression of NT-3 and IL-1βin DRG and spinal cord of CCI rats; we also examined the expression of spinal GFAP and OX-42 in spinal cord. In present study, the MWT and TWL of CCI group rats were lower than those in the Sham CCI group rats, but EA treatment increased the pain thresholds. Furtherly, we found that EA upregulates the expression of NT-3 in DRG and spinal cord of CCI rats, while EA downregulates the expression of IL-1β. Additionally, immunofluorescence exhibited that CCI-induced activation of microglia and astrocytes was inhibited significantly by EA treatment. These results demonstrated that the analgesic effect of EA may be achieved through promoting the neural protection of NT-3 as well as the inhibition of IL-1βproduction and spinal glial activity.

scholarly journals Effects of Hyperbaric Oxygen on Pain-Related Behaviours and Nitric Oxide Synthase Expression in a Rat Model of Neuropathic Pain

2013 ◽  
Vol 18 (3) ◽  
pp. 137-141 ◽  
Author(s):  
Guang Han ◽  
Lu Li ◽  
Ling-xin Meng
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Neuropathic Pain ◽  
Nitric Oxide Synthase ◽  
Hyperbaric Oxygen ◽  
Rat Model ◽  
Withdrawal Threshold ◽  
Withdrawal Latency ◽  
Oxide Synthase ◽  
Inducible Nos

BACKGROUND: Neuropathic pain is complex, and a satisfactory therapeutic method of treatment has yet to be developed; therefore, finding a new and effective therapeutic method is an important issue in the field of neuropathic pain.OBJECTIVE: To determine the effects of hyperbaric oxygen (HBO) on pain-related behaviours and nitric oxide synthase (NOS) expression in a rat model of neuropathic pain.METHODS: Forty male Sprague Dawley rats were randomly divided into five groups (eight rats per group) including control, sham operation, sciatic nerve with chronic constriction injury (CCI), HBO pretreatment (pre-HBO) and HBO post-treatment (post-HBO) groups. Pain-related behaviours and NOS expression in the spinal cord were compared among the five groups.RESULTS: Compared with the CCI group, the mechanical withdrawal threshold was significantly increased and thermal withdrawal latency was significantly extended in the pre-HBO and post-HBO groups (all P<0.05). After CCI, expression of spinal neuronal NOS and inducible NOS were increased. Expression of spinal neuronal NOS and inducible NOS were significantly decreased in the pre-HBO and post-HBO groups compared with the CCI group (all P<0.05). Spinal eNOS expression changed very little.DISCUSSION: HBO has been used as an effective and noninvasive method for the treatment of spinal cord injuries and high-altitude sickness, and in immunosuppression and stem-cell research; however, it has yet to be applied to the treatment of neuropathic pain. The present study indicated that HBO effectively increased mechanical withdrawal threshold and thermal withdrawal latency, demonstrating that HBO has therapeutic effects on neuropathic pain.CONCLUSION: HBO inhibits pain in rats with CCI through the regulation of spinal NOS expression.

scholarly journals Interferon-β suppresses inflammatory pain through activating µ-opioid receptor

2021 ◽  
Vol 17 ◽  
pp. 174480692110452
Author(s):  
Chien Cheng Liu ◽  
I Cheng Lu ◽  
Li Kai Wang ◽  
Jen Yin Chen ◽  
Yu Yu Li ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Western Blot ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Inflammatory Pain ◽  
Analgesic Effect ◽  
Intrathecal Injection ◽  
Type I ◽  
Withdrawal Threshold ◽  
Withdrawal Latency

Interferons (IFNs) are cytokines secreted by infected cells that can interfere with viral replication. Besides activating antiviral defenses, type I IFNs also exhibit diverse biological functions. IFN-β has been shown to have a protective effect against neurotoxic and inflammatory insults on neurons. Therefore, we aimed to investigate the possible role of IFN-β in reducing mechanical allodynia caused by Complete Freund’s Adjuvant (CFA) injection in rats. We assessed the antinociceptive effect of intrathecal IFN-β in naïve rats and the rats with CFA–induced inflammatory pain. After the behavioral test, the spinal cords of the rats were harvested for western blot and immunohistochemical double staining. We found that intrathecal administration of IFN-β in naïve rats can significantly increase the paw withdrawal threshold and paw withdrawal latency. Further, the intrathecal injection of a neutralizing IFN-β antibody can reduce the paw withdrawal threshold and paw withdrawal latency, suggesting that IFN-β is produced in the spinal cord in normal conditions and serves as a tonic inhibitor of pain. In addition, intrathecal injection of IFN-β at dosages from 1000 U to 10000 U demonstrates a significant transient dose-dependent inhibition of CFA-induced inflammatory pain. This analgesic effect is reversed by intrathecal naloxone, suggesting that IFN-β produces an analgesic effect through central opioid receptor-mediated signaling. Increased expression of phospho-µ-opioid receptors after IFN-β injection was observed on western blot, and immunohistochemical staining showed that µ-opioids co-localized with IFN-α/βR in the dorsal horn of the spinal cord. The findings of this study demonstrate that the analgesic effect of IFN-β is through µ-opioid receptors activation in spial cord.

scholarly journals Synaptotagmin 1 Is Involved in Neuropathic Pain and Electroacupuncture-Mediated Analgesic Effect

2020 ◽  
Vol 21 (3) ◽  
pp. 968 ◽  
Author(s):  
Juan Wan ◽  
Sha Nan ◽  
Jingjing Liu ◽  
Mingxing Ding ◽  
Hongmei Zhu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Analgesic Effect ◽  
Spared Nerve Injury ◽  
Withdrawal Threshold ◽  
Protein Levels ◽  
Qrt Pcr ◽  
Withdrawal Latency ◽  
Different Temperatures ◽  
Synaptotagmin 1 ◽  
Sirna Silencing

Numerous studies have verified that electroacupuncture (EA) can relieve neuropathic pain through a variety of mechanisms. Synaptotagmin 1 (Syt-1), a synaptic vesicle protein for regulating exocytosis of neurotransmitters, was found to be affected by EA stimulation. However, the roles of Syt-1 in neuropathic pain and EA-induced analgesic effect remain unclear. Here, the effect of Syt-1 on nociception was assessed through an antibody blockade, siRNA silencing, and lentivirus-mediated overexpression of spinal Syt-1 in rats with spared nerve injury (SNI). EA was used for stimulating bilateral “Sanjinjiao” and “Zusanli” acupoints of the SNI rats to evaluate its effect on nociceptive thresholds and spinal Syt-1 expression. The mechanically and thermally nociceptive behaviors were assessed with paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) at different temperatures, respectively, at day 0, 7, 8, 14, and 20. Syt-1 mRNA and protein levels were determined with qRT-PCR and Western blot, respectively, and its distribution was observed with the immunohistochemistry method. The results demonstrated Syt-1 antibody blockade and siRNA silencing increased ipsilateral PWTs and PWLs of SNI rats, while Syt-1 overexpression decreased ipsilateral PWTs and PWLs of rats. EA significantly attenuated nociceptive behaviors and down-regulated spinal Syt-1 protein levels (especially in laminae I-II), which were reversed by Syt-1 overexpression. Our findings firstly indicate that Syt-1 is involved in the development of neuropathic pain and that EA attenuates neuropathic pain, probably through suppressing Syt-1 protein expression in the spinal cord.

One-Year Outcomes of Spinal Cord Stimulation of the Dorsal Root Ganglion in the Treatment of Chronic Neuropathic Pain

2014 ◽  
Vol 18 (1) ◽  
pp. 41-49 ◽  
Author(s):  
Liong Liem ◽  
Marc Russo ◽  
Frank J.P.M. Huygen ◽  
Jean-Pierre Van Buyten ◽  
Iris Smet ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Spinal Cord Stimulation ◽  
Dorsal Root ◽  
Chronic Neuropathic Pain ◽  
One Year ◽  
Stimulation Of

A Prospective Analysis of Neuromonitoring for Confirmation of Lead Placement in Dorsal Root Ganglion Stimulation

2017 ◽  
Vol 14 (6) ◽  
pp. 654-660 ◽  
Author(s):  
Steven M Falowski ◽  
Andreas Dianna
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Evoked Potential ◽  
Somatosensory Evoked Potential ◽  
Prospective Analysis ◽  
Awake Patient ◽  
Chronic Neuropathic Pain ◽  
Lead Placement

Abstract BACKGROUND Dorsal root ganglion stimulation is a neuromodulation therapy used for chronic neuropathic pain. Typically, patients are awakened intraoperatively to confirm adequate placement. OBJECTIVE To determine whether neuromonitoring can confirm placement in an asleep patient. METHODS This is a prospective analysis of 12 leads placed in 6 patients. Lead confirmation was confirmed by awake intraoperative testing, as well as asleep testing utilizing neuromonitoring. Patients were used as their own control. Sensory and motor thresholds for each patient with awake and asleep neuromonitoring testing were recorded. Intraoperative impedance and postoperative programming were also recorded. RESULTS In each patient, paresthesias were generated prior to motor contractions in the awake patient. For each patient, somatosensory evoked potential responses were present after lowering below the dropout threshold of electromyogram responses with neuromonitoring. There were varying degrees of separation in the thresholds that did not appear to be consistent across level or diagnosis. Smaller degrees of separation between thresholds during awake testing also held true in the asleep patient. This was further confirmed with postoperative programming. Impedances did not alter the separation in thresholds or amount of stimulation required for responses. One patient was combative during awake testing, and therefore motor thresholds were not obtained. This same patient was determined to have a ventral placement, confirmed with awake and asleep neuromonitoring testing. CONCLUSION This series demonstrates that the proposed neuromonitoring protocol can be used in an asleep patient to assure proper positioning of the dorsal root ganglion electrode in the dorsal foramen by generating somatosensory evoked potential responses in the absence of electromyogram responses.

Spinal Endogenous Acetylcholine Contributes to the Analgesic Effect of Systemic Morphine in Rats

2001 ◽  
Vol 95 (2) ◽  
pp. 525-530 ◽  
Author(s):  
Shao-Rui Chen ◽  
Hui-Lin Pan
Keyword(s):  
Spinal Cord ◽  
Receptor Antagonist ◽  
Analgesic Effect ◽  
Antinociceptive Effect ◽  
Intrathecal Injection ◽  
Radiant Heat ◽  
Cholinergic Receptor ◽  
Inhibitory Effect ◽  
Withdrawal Latency ◽  
Aziridinium Ion

Background Systemic morphine is known to cause increased release of acetyicholine in the spinal cord. Intrathecal injection of the cholinergic receptor agonists or acetyicholinesterase inhibitors produces antinociception in both animals and humans. In the present study, we explored the functional importance of spinal endogenous acetylcholine in the analgesic action produced by intravenous morphine. Methods Rats were implanted with intravenous and intrathecal catheters. The antinociceptive effect of morphine was determined by the paw-withdrawal latency in response to a radiant heat stimulus after intrathecal treatment with atropine (a muscarinic receptor antagonist), mecamylamine (a nicotinic receptor antagonist), or cholinergic neurotoxins (ethylcholine mustard aziridinium ion [AF64A] and hemicholinium-3). Results Intravenous injection of 2.5 mg/kg morphine increased significantly the paw-withdrawal latency. Intrathecal pretreatment with 30 microg atropine (n = 7) or 50 microg mecamylamine (n = 6) both attenuated significantly the antinociceptive effect of morphine. The inhibitory effect of atropine on the effect of morphine was greater than that of mecamylanilne. Furthermore, the antinociceptive effect of morphine was significantly reduced in rats pretreated with intrathecal AF64A (n = 7) or hemicholinium-3 (n = 6) to inhibit the high-affinity choline transporter and acetylcholine synthesis. We found that intrathecal AF64A reduced significantly the [3H]hemicholinium-3 binding sites but did not affect its affinity in the dorsal spinal cord. Conclusions The data in the current study indicate that spinal endogenous acetylcholine plays an important role in mediating the analgesic effect of systemic morphine through both muscarinic and nicotinic receptors.

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