scholarly journals Effect of Electroacupuncture on Rats with Chronic Constriction Injury-Induced Neuropathic Pain

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Hsin-Cheng Hsu ◽  
Nou-Ying Tang ◽  
Yi-Wen Lin ◽  
Tsai-Chung Li ◽  
Hsu-Jan Liu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Transient Receptor Potential ◽  
Chronic Constriction Injury ◽  
Receptor Potential ◽  
Radiant Heat ◽  
Transient Receptor Potential Vanilloid ◽  
Sd Rats ◽  
Transient Receptor ◽  
The Right ◽  
The Relationship

We adopt the chronic constriction injury (CCI) model to induce neuropathic pain to Spragrue-Dawley (SD) rats by ligating the right sciatic nerve of using four 4-0 chromic gut sutures and subsequently applying 2 and 15 Hz electroacupuncture (EA), respectively, to the right (ipsilateral) Zusanli (St-36) and Shangjuxu (St-37) acupoints. The results of this study are summarized as follows: (1) the differences in withdrawal latencies for the radiant heat test and total lift leg counts for the cold plate test (4°C) of the control (i.e., non-EA) and sham groups were greater than those of the 2 Hz EA (2EA) and 15 Hz EA (15EA) groups; (2) the von Frey test filament gram counts of the control and sham groups were less than those of the 2EA and 15EA groups on the 6th, 7th, 8th, 11th, 12th, and 13th day following ligation; and (3) the 2EA and 15EA groups exhibited reduced cerebral transient receptor potential vanilloid type 4 (TRPV4) expressions, although we did not observe a similar effect for cerebral TRPV1 or spinal TRPV4/TRPV1 expressions. These findings show that 2 and 15 Hz EA can reduce CCI-induced neuropathic pain, which indicates that various spinal segmental and gate effects have a crucial function in pain reduction. The relationship between EA and TRPV4/TRPV1 expression requires further study.

scholarly journals The Calcium Channel α2δ1 Subunit: Interactional Targets in Primary Sensory Neurons and Role in Neuropathic Pain

2021 ◽  
Vol 15 ◽  
Author(s):  
Wenqiang Cui ◽  
Hongyun Wu ◽  
Xiaowen Yu ◽  
Ting Song ◽  
Xiangqing Xu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Calcium Channel ◽  
Sensory Neurons ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Peripheral Sensitization ◽  
Primary Sensory Neurons ◽  
Transient Receptor ◽  
Underlying Mechanisms

Neuropathic pain is mainly triggered after nerve injury and associated with plasticity of the nociceptive pathway in primary sensory neurons. Currently, the treatment remains a challenge. In order to identify specific therapeutic targets, it is necessary to clarify the underlying mechanisms of neuropathic pain. It is well established that primary sensory neuron sensitization (peripheral sensitization) is one of the main components of neuropathic pain. Calcium channels act as key mediators in peripheral sensitization. As the target of gabapentin, the calcium channel subunit α2δ1 (Cavα2δ1) is a potential entry point in neuropathic pain research. Numerous studies have demonstrated that the upstream and downstream targets of Cavα2δ1 of the peripheral primary neurons, including thrombospondins, N-methyl-D-aspartate receptors, transient receptor potential ankyrin 1 (TRPA1), transient receptor potential vanilloid family 1 (TRPV1), and protein kinase C (PKC), are involved in neuropathic pain. Thus, we reviewed and discussed the role of Cavα2δ1 and the associated signaling axis in neuropathic pain conditions.

Repeated capsaicin patch applications in patients with localized peripheral neuropathic pain

Ból ◽  
2021 ◽  
Vol 22 (1) ◽  
pp. 56-65
Author(s):  
Małgorzata Malec-Milewska ◽  
Jerzy Wordliczek ◽  
Renata Zajączkowska
Keyword(s):  
Neuropathic Pain ◽  
Transient Receptor Potential ◽  
Significant Proportion ◽  
Case Series ◽  
Receptor Potential ◽  
The Body ◽  
Transient Receptor Potential Vanilloid ◽  
Transient Receptor ◽  
Good Treatment Option ◽  
Localized Neuropathic Pain

Neuropathic pain is still a challenging problem. It is experienced by millions of people worldwide, with an approximate prevalence of 7‒10% in the general population. Despite the availability of a variety of treatment methods, a significant proportion of patients suffer from poorly controlled neuropathic pain. Capsaicin is a highly selective TRPV1 (Transient Receptor Potential Vanilloid Type 1) agonist. When applied topically, it leads to the defunctionalisation of hyperactive nociceptive receptors, temporary destruction of peripheral nerve endings, and a significant reduction or cessation of pain. Therefore 8% capsaicin patches are used to treat several peripheral, localized neuropathic pain syndromes. The study aimed to present a case series of patients suffering from peripheral, localized neuropathic pain in case the use of repeated applications of 8% capsaicin patches significantly reduced the intensity of pain. In 5 out of 6 patients we observed a gradual extension of the pain relief period until the pain disappeared, which led to the reduction or discontinuation of systemic pharmacotherapy. In summary, a therapy limited to a certain area of the body, without potential systemic adverse effects, which requires repetition at fairly long intervals, appears to be a good treatment option.

scholarly journals Pirt Together with TRPV1 Is Involved in the Regulation of Neuropathic Pain

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Changming Wang ◽  
Leying Gu ◽  
Yonglan Ruan ◽  
Tana Gegen ◽  
Lei Yu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Transient Receptor Potential ◽  
Life Quality ◽  
Thermal Hyperalgesia ◽  
In Vitro Study ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Cci Model ◽  
Transient Receptor

Neuropathic pain is a chronic pain and reduces the life quality of patients substantially. Transient receptor potential vanilloid channel 1 (TRPV1), a nonselective cation channel, has been shown to play a crucial role in neuropathic pain. Although TRPV1 plays an important role in neuropathic pain, the mechanism of how TRPV1 was regulated in neuropathic pain remains unclear. Pirt is a membrane protein and binds to TRPV1 to enhance its activity. It was suggested that Pirt should also be involved in neuropathic pain. In this study, we investigated the role of Pirt in neuropathic pain (CCI model); the results show that mechanical allodynia and thermal hyperalgesia were alleviated in Pirt−/− mice in CCI models. TRPV1 expression was increased by immunofluorescence and real-time PCR experiments. The increase in TRPV1 expression was less in Pirt knockout mice in CCI models. Moreover, the number of capsaicin-responding neurons and the magnitude of evoked calcium response were attenuated in DRG neurons from Pirt−/− mice in CCI models. Finally, we found that the pain behavior attenuated in dysfunction of both Pirt and TRPV1 was much stronger than in dysfunction of Pirt or TRPV1 only in a CCI model in vitro study. Taken together, Pirt together with TRPV1 is involved in CCI-induced neuropathic pain.

scholarly journals Suppression of TRPV1/TRPM8/P2Y Nociceptors by Withametelin via Downregulating MAPK Signaling in Mouse Model of Vincristine-Induced Neuropathic Pain

2021 ◽  
Vol 22 (11) ◽  
pp. 6084
Author(s):  
Adnan Khan ◽  
Bushra Shal ◽  
Ashraf Ullah Khan ◽  
Rahim Ullah ◽  
Muhammad Waleed Baig ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Sciatic Nerve ◽  
Transient Receptor Potential ◽  
Purinergic Receptor ◽  
Receptor Potential ◽  
B Cell Lymphoma ◽  
Mapk Signaling ◽  
Transient Receptor Potential Vanilloid ◽  
Transient Receptor

Vincristine (VCR) is a widely used chemotherapy drug that induced peripheral painful neuropathy. Yet, it still lacks an ideal therapeutic strategy. The transient receptor potential (TRP) channels, purinergic receptor (P2Y), and mitogen-activated protein kinase (MAPK) signaling play a crucial role in the pathogenesis of neuropathic pain. Withametelin (WMT), a potential Phytosteroid isolated from datura innoxa, exhibits remarkable neuroprotective properties. The present investigation was designed to explore the effect of withametelin on VCR-induced neuropathic pain and its underlying molecular mechanism. Initially, the neuroprotective potential of WMT was confirmed against hydrogen peroxide (H2O2)-induced PC12 cells. To develop potential candidates for neuropathic pain treatment, a VCR-induced neuropathic pain model was established. Vincristine (75 μg/kg) was administered intraperitoneally (i.p.) for 10 consecutive days (day 1–10) for the induction of neuropathic pain. Gabapentin (GBP) (60 mg/kg, i.p.) and withametelin (0.1 and 1 mg/kg i.p.) treatments were given after the completion of VCR injection on the 11th day up to 21 days. The results revealed that WMT significantly reduced VCR-induced pain hypersensitivity, including mechanical allodynia, cold allodynia, and thermal hyperalgesia. It reversed the VCR-induced histopathological changes in the brain, spinal cord, and sciatic nerve. It inhibited VCR-induced changes in the biochemical composition of the myelin sheath of the sciatic nerve. It markedly downregulated the expression levels of TRPV1 (transient receptor potential vanilloid 1); TRPM8 (Transient receptor potential melastatin 8); and P2Y nociceptors and MAPKs signaling, including ERK (Extracellular Signal-Regulated Kinase), JNK (c-Jun N-terminal kinase), and p-38 in the spinal cord. It suppressed apoptosis by regulating Bax (Bcl2-associated X-protein), Bcl-2 (B-cell-lymphoma-2), and Caspase-3 expression. It considerably attenuated inflammatory cytokines, oxidative stress, and genotoxicity. This study suggests that WMT treatment suppressed vincristine-induced neuropathic pain by targeting the TRPV1/TRPM8/P2Y nociceptors and MAPK signaling.

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