scholarly journals Effect of Electroacupuncture at ST36 on Gastric-Related Neurons in Spinal Dorsal Horn and Nucleus Tractus Solitarius

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Xiaoyu Wang ◽  
Hong Shi ◽  
Hongyan Shang ◽  
Wei He ◽  
Shuli Chen ◽  
...  

The aim of this study was to observe the effect of electroacupuncture (EA) at the ST36 acupoint on the firing rate of gastric-related neurons in the spinal dorsal horn (SDH) and nucleus tractus solitarius (NTS). There were different effects of gastric distention in SDH and NTS in 46 male Sprague-Dawley rats. In 10 excitatory neurons in SDH, most of the neurons were inhibited by homolateral EA. The firing rates decreased significantly (P<0.05) in 10 excitatory gastric-related neurons in NTS; the firing rates of 6 neurons were further excited by homolateral EA, with a significant increase of the firing rates (P<0.05); all inhibitory gastric-related neurons in NTS were excited by EA. The inhibition rate of homolateral EA was significantly increased in comparison with contralateral EA in gastric-related neurons of SDH (P<0.05). There was no significant difference between homolateral and contralateral EA in gastric-related neurons of NTS. EA at ST36 changes the firing rate of gastric-related neurons in SDH and NTS. However, there are some differences in responsive mode in these neurons. The existence of these differences could be one of the physiological foundations of diversity and complexity in EA effects.

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Zhenyu Wu ◽  
Xiaofang Lu ◽  
Shengsheng Zhang ◽  
Chunyang Zhu

The present study investigated the effect of Chinese medicine Sini-San (SNS) on visceral hypersensitivity in a rat model of functional dyspepsia (FD), and it explored related underlying mechanisms. The rat model of FD was developed by combining neonatal iodoacetamide (IA) treatment and adult tail-clamping. After SNS treatment, the behavior and electromyographic testing were performed to evaluate the visceromotor responses of rats to gastric distention. Immunofluorescence was used to detect the distribution of iNOS-positive cells in the spinal dorsal horn, while the real-time quantitative PCR and western blot were used for detection of the gene expression of c-fos, iNOS, and GABAb and protein levels of iNOS and GABAb in the spinal dorsal horn, respectively. The protein concentration of cGMP and PKG proteins in the spinal dorsal horn were quantified by enzyme-linked immunosorbent assay. In this study, SNS treatment significantly reduced the behavioral score and electromyographic response to graded intragastric distension pressure. The middle-dose of SNS treatment significantly reduced the distribution of iNOS-positive cells in the spinal dorsal horn of FD model rats. The gene expression of c-fos, iNOS, and GABAb and the protein contents of iNOS, GABAb, cGMP, and PKG in the spinal dorsal horn of FD model rats were restored to a normal level by middle-dose of SNS treatment. Our results suggest that Sini-San may alleviate the visceral hypersensitivity in FD model rats via regulation of the NO/cGMP/PKG pathway in the spinal dorsal horn.


2014 ◽  
Vol 32 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Tao Zhou ◽  
Jiang Wang ◽  
Chun-Xiao Han ◽  
Ishida Torao ◽  
Yi Guo

Objectives Previous research has suggested that different manual acupuncture (MA) manipulations may have different physiological effects. Recent studies have demonstrated that neural electrical signals are generated or changed when acupuncture is administered. In order to explore the effects of different MA manipulations on the neural system, an experiment was designed to record the discharges of wide dynamic range (WDR) neurons in the spinal dorsal horn evoked by MA at different frequencies (0.5, 1, 2 and 3 Hz) at ST36. Methods Microelectrode extracellular recordings were used to record the discharges of WDR neurons evoked by different MA manipulations. Approximate firing rate and coefficient of variation of interspike interval (ISI) were used to extract the characteristic parameters of the neural electrical signals after spike sorting, and the neural coding of the evoked discharges by different MA manipulations was obtained. Results Our results indicated that the neuronal firing rate and time sequences of ISI showed distinct clustering properties for different MA manipulations, which could distinguish them effectively. Conclusions The combination of firing rate and ISI codes carries information about the acupuncture stimulus frequency. Different MA manipulations appear to change the neural coding of electrical signals in the spinal dorsal horn through WDR neurons.


2005 ◽  
Vol 102 (1) ◽  
pp. 165-174 ◽  
Author(s):  
Mikito Kawamata ◽  
Eichi Narimatsu ◽  
Yuji Kozuka ◽  
Toshiyuki Takahashi ◽  
Shigekazu Sugino ◽  
...  

Background The aim of this study was to determine whether halothane and isoflurane used during and after surgical injury attenuate subsequent hyperexcitability of spinal dorsal horn (SDH) neurons by preventing development of central sensitization. Methods Activity of a wide-dynamic-range neuron of the SDH was isolated in decerebrate-spinal Sprague-Dawley rats, and neuronal activity (receptive field size and responses to nonnoxious and noxious stimuli) was recorded. A 1-cm-long incision was made through the skin, fascia, and muscle under anesthesia with halothane (1.1% or 2.2%) and isoflurane (1.4% or 2.8%). Anesthesia was discontinued just after the incision had been made or was continued until 30 min after the incision, and activity of the SDH neurons was measured for up to 2 h after the incision. In a control group, the incision was made without anesthesia. Results In the control group, the incision resulted in maximum excitation in the SDH neurons during surgery; spontaneous activity significantly increased for up to 30 min after the incision (P &lt; 0.05) but did not significantly increase thereafter, returning to the preincision value. Halothane and isoflurane suppressed excitation of the neurons during the incision in a concentration-related manner. Administration of 2.2% halothane and 2.8% isoflurane during the incision and for up to 30 min after the incision almost abolished activity of the neurons for 30 min after the incision. The magnitude of neuronal activity 2 h after the incision was not significantly different among all groups, including the control group. Conclusions The results demonstrate that administration of halothane and isoflurane does not attenuate development of hyperexcitability of SDH neurons despite the fact that excitation and spontaneous activity during and after the incision were greatly suppressed by administration of halothane and isoflurane.


2021 ◽  
pp. 096452842110207
Author(s):  
Ying Jin ◽  
Jie Zhou ◽  
Fangfang Xu ◽  
Zeqin Ren ◽  
Jun Hu ◽  
...  

Background: Hyperalgesic priming (HP) is a model of the transition from acute to chronic pain. Electroacupuncture (EA) could inhibit pain development through the peripheral dorsal root ganglia; however, it is unclear whether it can mitigate the transition from acute to chronic pain by attenuating protein expression in the p38 MAPK (mitogen-activated protein kinase)/tumour necrosis factor alpha (TNF-α) pathway in the spinal dorsal horn. Aims: We aimed to determine whether EA could prevent the transition from acute to chronic pain by affecting the p38 MAPK/TNF-α pathway in the spinal dorsal horn in a rat model established using HP. Methods: We first randomly subdivided 30 male Sprague-Dawley (SD) rats into 5 groups ( n = 6 per group): control (N), sham HP (Sham-HP), HP, HP + SB203580p38 MAPK (HP+SB203580), and HP + Lenalidomide (CC-5013) (HP+Lenalidomide). We then randomly subdivided a further 30 male SD rats into 5 groups ( n = 6 per group): Sham-HP, HP, sham EA (Sham EA), EA (EA), and EA + U-46619 p38 MAPK agonist (EA+U-46619). We assessed the effects of EA on the mechanical paw withdrawal threshold and p38 MAPK/TNF-α expression in the spinal dorsal horn of rats subjected to chronic inflammatory pain. Results: Rats in the EA group had reduced p38 MAPK and TNF-α expression and had significantly reduced mechanical hyperalgesia compared with rats in the other groups. Conclusion: Our findings indicate that EA could increase the mechanical pain threshold in rats and inhibit the transition from acute pain to chronic pain. This mechanism could involve reduced p38 MAPK/TNF-α expression in the spinal dorsal horn.


Pharmacology ◽  
2018 ◽  
Vol 102 (5-6) ◽  
pp. 300-306 ◽  
Author(s):  
Chang-Cheng Lv ◽  
Man-Li Xia ◽  
Shu-Juan Shu ◽  
Fei Chen ◽  
Li-Shan Jiang

Remifentanil-induced hyperalgesia (RIH) is known to be associated with oxidative stress and inflammation. Betulinic acid (BA) was reported to reduce visceral pain owing to its anti-oxidative and anti-inflammatory potential. Here, we ­explored whether BA can attenuate RIH through inhibiting oxidative stress and inflammation in spinal dorsal horn. Sprague-Dawley rats were randomly divided into 4 groups: Control, Incision, RIH, and RIH pre-treated with BA. After pretreated with BA (25 mg/kg, i.g.) for 7 days, rats were subcutaneously infused with remifentanil (40 μg/kg) for 30 min during right plantar incision surgery to induce RIH. The paw withdrawal mechanical threshold (PWMT), paw withdrawal thermal latency (PWTL), spinal oxidative stress and inflammatory mediators were determined. Intraoperative remifentanil infusion induced postoperative hyperalgesia, as evidenced by the significant decrease in PWMT and PWTL (p < 0.01), and the significant increase in oxidative stress and inflammation evidenced by up-regulations of malondialdehyde, 3-nitrotyrosine, interleukin-1β and tumour necrosis factor-α (p < 0.01) in spinal dorsal horn and matrix metalloproteinase-9 (MMP-9) activity (p < 0.01) in dorsal root ganglion, as well as a decrease in manganese superoxide ­dismutase activity (p < 0.01) compared with control and ­incision groups. All these results mentioned above were markedly reversed by pre-treatment with BA (p < 0.01) compared with RIH group. These findings demonstrated that BA can effectively attenuate RIH, which associates with potentially inhibiting oxidative stress and subsequently down-regulating MMP-9-related pro-inflammatory cyokines in spinal dorsal horn.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Hong Liu ◽  
Weidong Li ◽  
Binbing Xu ◽  
Jiduan Jiang ◽  
Yuanyuan Zhang ◽  
...  

Objective. To observe the changes in the mechanical withdrawal threshold (MWT) and the proportion of GABA-immunoreactive neurons in spinal dorsal horn (SDH) of the spared nerve injury (SNI) rat model. Methods. Thirty-six healthy male SD rats were randomly divided into a sham-operated group (group D, n = 18 ) and an SNI group (group S, n = 18 ). The left sciatic nerve trunk and three branches were exposed, two of which, known as tibial and the peroneal nerve, were ligated and cut off. The sural nerve was preserved to build the SNI model in group S. The left sciatic nerve trunk and three branches were only exposed in group D. MWT tests were performed on the medial and lateral sides of the rats’ left hindpaw 1 day before surgery and at 7th, 14th, and 28th day after surgery. Results. In group S, compared with the baseline measured 1 day before surgery, MWT on the medial and lateral sides of the rats’ left hindpaw decreased significantly on the 7th, 14th, and 28th days after surgery ( P < 0.05 ), while in group D, there was no statistically significant difference ( P > 0.05 ). Compared with right SDH, there were not statistically significant reductions in the proportions of GABAergic neurons of left SDH on 7th and 28th day after SNI ( P > 0.05 ); however, the proportion of GABAergic neurons in left SDH significantly decreased, compared with that in right side on 14th day after SNI ( P < 0.05 ). On the same way, the proportions of GABAergic neurons on 7th, 14th, and 28th day after surgery were not statistically different ( P > 0.05 ) in group D. Conclusion. The SNI model could reduce the proportion of GABA-immunoreactive neurons in the rat’s spinal dorsal horn on the nerve-injured side, and this change was lasting, which might be related to the transformation of the GABA-immunoreactive neurons.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Qi An ◽  
Chenyan Sun ◽  
Ruidi Li ◽  
Shuhui Chen ◽  
Xinpei Gu ◽  
...  

Abstract Background Calcitonin gene-related peptide (CGRP) as a mediator of microglial activation at the transcriptional level may facilitate nociceptive signaling. Trimethylation of H3 lysine 27 (H3K27me3) by enhancer of zeste homolog 2 (EZH2) is an epigenetic mark that regulates inflammatory-related gene expression after peripheral nerve injury. In this study, we explored the relationship between CGRP and H3K27me3 in microglial activation after nerve injury, and elucidated the underlying mechanisms in the pathogenesis of chronic neuropathic pain. Methods Microglial cells (BV2) were treated with CGRP and differentially enrichments of H3K27me3 on gene promoters were examined using ChIP-seq. A chronic constriction injury (CCI) rat model was used to evaluate the role of CGRP on microglial activation and EZH2/H3K27me3 signaling in CCI-induced neuropathic pain. Results Overexpressions of EZH2 and H3K27me3 were confirmed in spinal microglia of CCI rats by immunofluorescence. CGRP treatment induced the increased of H3K27me3 expression in the spinal dorsal horn and cultured microglial cells (BV2) through EZH2. ChIP-seq data indicated that CGRP significantly altered H3K27me3 enrichments on gene promoters in microglia following CGRP treatment, including 173 gaining H3K27me3 and 75 losing this mark, which mostly enriched in regulation of cell growth, phagosome, and inflammation. qRT-PCR verified expressions of representative candidate genes (TRAF3IP2, BCL2L11, ITGAM, DAB2, NLRP12, WNT3, ADAM10) and real-time cell analysis (RTCA) verified microglial proliferation. Additionally, CGRP treatment and CCI increased expressions of ITGAM, ADAM10, MCP-1, and CX3CR1, key mediators of microglial activation in spinal dorsal horn and cultured microglial cells. Such increased effects induced by CCI were suppressed by CGRP antagonist and EZH2 inhibitor, which were concurrently associated with the attenuated mechanical and thermal hyperalgesia in CCI rats. Conclusion Our findings highly indicate that CGRP is implicated in the genesis of neuropathic pain through regulating microglial activation via EZH2-mediated H3K27me3 in the spinal dorsal horn.


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