scholarly journals Comparison of Painful Response to Mechanical Stimulation of the Plantar and Dorsal Surface of Paw Following Chronic Constriction Injury-induced Neuropathic Pain

2021 ◽  
Vol 11 (3) ◽  
pp. 327-332
Author(s):  
Ali Ghanbari ◽  
Mohadeseh Mohammadi
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Stimulation ◽  
Sham Group ◽  
Chronic Constriction Injury ◽  
Dorsal Surface ◽  
Plantar Surface ◽  
Withdrawal Threshold ◽  
Post Surgery ◽  
Withdrawal Response ◽  
Stimulation Of

Mechanical and thermal stimuli were used to evaluate neuropathic pain-like behavior in animal models usually. Mechanical stimulation of paw plantar surface is commonly used to determine mechanical allodynia. In the present study, paw withdrawal response to plantar surface stimulation was compared with paw withdrawal response to dorsal surface stimulation. To this end, a total of 30 female Wistar rats (180-220 g), were assigned randomly to three groups as intact (without any manipulation), sham (incision of skin and muscles without nerve injury), and neuropathy (sciatic nerve lesion) with 10 in each group. To induction of neuropathy (chronic constriction injury), four movable ligations were established around the sciatic nerve using catgut chromic suture with a distance of one millimeter apart and then wound incision was closed. In the sham group, the incision site was closed without nerve ligation. Mechanical allodynia was examined by Von Frey filaments for four weeks. The findings indicated that the paw withdrawal threshold following dorsal surface stimulation was significantly reduced compared to the sham group at day 21 post-surgery. Moreover, paw withdrawal threshold following plantar surface stimulation significantly decreased compared to the sham group at day 21 post-surgery. The present results regarding the sham group showed that the paw withdrawal threshold after mechanical stimulation of the plantar surface was not significantly different from that of the dorsal surface paw. In addition, and there was no significant difference between the paw withdrawal response to plantar surface and dorsal one. In conclusion, paw withdrawal threshold to plantar surface mechanical stimulation was not significantly different from one in dorsal surface following neuropathic pain induced by chronic constriction injury.

Identification of Mechanoafferent Neurons in Terrestrial Snail: Response Properties and Synaptic Connections

2002 ◽  
Vol 87 (5) ◽  
pp. 2364-2371 ◽  
Author(s):  
Aleksey Y. Malyshev ◽  
Pavel M. Balaban
Keyword(s):  
Avoidance Behavior ◽  
Receptive Fields ◽  
Dorsal Surface ◽  
Mechanical Stimulus ◽  
Terrestrial Snail ◽  
Mechanosensory Neurons ◽  
Intracellular Stimulation ◽  
Pleural Ganglion ◽  
Withdrawal Response ◽  
Stimulation Of

In this study, we describe the putative mechanosensory neurons, which are involved in the control of avoidance behavior of the terrestrial snail Helix lucorum. These neurons, which were termed pleural ventrolateral (PlVL) neurons, mediated part of the withdrawal response of the animal via activation of the withdrawal interneurons. Between 15 and 30 pleural mechanosensory neurons were located on the ventrolateral side of each pleural ganglion. Intracellular injection of neurobiotin revealed that all PlVL neurons sent their axons into the skin nerves. The PlVL neurons had no spontaneous spike activity or fast synaptic potentials. In the reduced “CNS-foot” preparations, mechanical stimulation of the skin covering the dorsal surface of the foot elicited spikes in the PlVL neurons without any noticeable prepotential activity. Mechanical stimulus-induced action potentials in these cells persisted in the presence of high-Mg2+/zero-Ca2+ saline. Each neuron had oval-shaped receptive field 5–20 mm in length located on the dorsal surface of the foot. Partial overlapping of the receptive fields of different neurons was observed. Intracellular stimulation of the PlVL neurons produced excitatory inputs to the parietal and pleural withdrawal interneurons, which are known to control avoidance behavior. The excitatory postsynaptic potentials (EPSPs) in the withdrawal interneurons were induced in 1:1 ratio to the PlVL neuron spikes, and spike-EPSP latency was short and highly stable. These EPSPs also persisted in the high-Mg2+/high-Ca2+ saline, suggesting monosynaptic connections. All these data suggest that PlVL cells were the primary mechanosensory neurons.

Effects on Peroneal Motoneurons of Cutaneous Afferents Activated by Mechanical or Electrical Stimulations

2000 ◽  
Vol 83 (6) ◽  
pp. 3209-3216 ◽  
Author(s):  
Jean-François Perrier ◽  
Boris Lamotte D'Incamps ◽  
Nezha Kouchtir-Devanne ◽  
Léna Jami ◽  
Daniel Zytnicki
Keyword(s):  
Electrical Stimulation ◽  
Mechanical Stimulation ◽  
Cutaneous Afferents ◽  
Postsynaptic Potentials ◽  
Electric Pulses ◽  
Plantar Surface ◽  
Cutaneous Reflex ◽  
Inhibitory Postsynaptic Potentials ◽  
Mixed Pattern ◽  
Stimulation Of

The postsynaptic potentials elicited in peroneal motoneurons by either mechanical stimulation of cutaneous areas innervated by the superficial peroneal nerve (SP) or repetitive electrical stimulation of SP were compared in anesthetized cats. After denervation of the foot sparing only the territory of SP terminal branches, reproducible mechanical stimulations were applied by pressure on the plantar surface of the toes via a plastic disk attached to a servo-length device, causing a mild compression of toes. This stimulus evoked small but consistent postsynaptic potentials in every peroneal motoneuron. Weak stimuli elicited only excitatory postsynaptic potentials (EPSPs), whereas increase in stimulation strength allowed distinction of three patterns of response. In about one half of the sample, mechanical stimulation or trains of 20/s electric pulses at strengths up to six times the threshold of the most excitable fibers in the nerve evoked only EPSPs. Responses to electrical stimulation appeared with 3–7 ms central latencies, suggesting oligosynaptic pathways. In another, smaller fraction of the sample, inhibitory postsynaptic potentials (IPSPs) appeared with an increase of stimulation strength, and the last fraction showed a mixed pattern of excitation and inhibition. In 24 of 32 motoneurons where electrical and mechanical effects could be compared, the responses were similar, and in 6 others, they changed from pure excitation on mechanical stimulation to mixed on electrical stimulation. With both kinds of stimulation, stronger stimulations were required to evoke inhibitory postsynaptic potentials (IPSPs), which appeared at longer central latencies than EPSPs, indicating longer interneuronal pathways. The similarity of responses to mechanical and electrical stimulation in a majority of peroneal motoneurons suggests that the effects of commonly used electrical stimulation are good predictors of the responses of peroneal motoneurons to natural skin stimulation. The different types of responses to cutaneous afferents from SP territory reflect a complex connectivity allowing modulations of cutaneous reflex responses in various postures and gaits.

Lidocaine activates autophagy of astrocytes and ameliorates chronic constriction injury-induced neuropathic pain

2020 ◽  
Author(s):  
Jiaqi Yuan ◽  
Yue Fei
Keyword(s):  
Cell Proliferation ◽  
Neuropathic Pain ◽  
Chronic Constriction Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Factor ◽  
Experimental Basis ◽  
Withdrawal Threshold ◽  
Withdrawal Latency ◽  
Tnf Α ◽  
Rat Astrocytes

Abstract Lidocaine is a commonly used drug to alleviate neuropathic pain (NP). This work aims to investigate the mechanism of lidocaine in alleviating NP. Chronic constriction injury (CCI) rats were established by surgery to induce NP. We observed the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) of rats. Immunofluorescence staining was performed to determine the LC3/glial fibrillary acidic protein (GFAP)-positive cells. Rat astrocytes were treated with lipopolysaccharide (LPS) to induce CCI, and then treated with lidocaine or 3-MA (autophagy inhibitor). CCK-8 was performed to detect cell proliferation. Western blot and enzyme-linked immunosorbent assay were performed to detect the level of protein and inflammatory factor. CCI rats exhibited a decrease of MWT and TWL, which was effectively abolished by lidocaine. Lidocaine enhanced the number of LC3/GFAP-positive cells in CCI rats. Moreover, lidocaine inhibited the expression of GFAP and p62, and enhanced LC3-II/LC3-I expression in the LPS-treated astrocytes. Lidocaine inhibited the level of TNF-α and IL-1β in the LPS-treated astrocytes. The influence conferred by lidocaine was effectively abolished by 3-MA. In conclusion, our work demonstrates that lidocaine activates autophagy of astrocytes and ameliorates CCI-induced NP. Thus, our study provides a further experimental basis for the mechanism of lidocaine to alleviate NP.

scholarly journals The Effect of Alternating Current Iontophoresis on Rats with the Chronic Constriction Injury to the Infraorbital Nerve

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Yoko Yamazaki ◽  
Masahiro Umino ◽  
Haruhisa Fukayama ◽  
Masahiko Shimada
Keyword(s):  
Chronic Constriction Injury ◽  
Animal Experiments ◽  
Physiological Saline ◽  
Infraorbital Nerve ◽  
Lidocaine Hydrochloride ◽  
Facial Skin ◽  
Trigeminal Nucleus ◽  
Withdrawal Threshold ◽  
Duration Of Efficacy ◽  
Stimulation Of

This study aimed to examine the effect of AC iontophoresis on rats with the chronic constriction injury (CCI) to the infraorbital nerve by animal experiments. CCI model rats were divided into four groups, namely, rats that received general anesthesia for 60 min except AC IOP (CCI:n=5), AC IOP with 0.9% physiological saline for 60 min (CCI + saline AC IOP:n=5), AC IOP with 4% lidocaine hydrochloride for 60 min (CCI + lidocaine AC IOP:n=5), and attachment of two electrodes soaked with 4% lidocaine hydrochloride to the facial skin for 60 min (CCI + attach lidocaine:n=5). In the CCI + lidocaine AC IOP group, an elevated withdrawal threshold was observed after AC IOP, and the duration of efficacy was longer compared with that in the CCI + saline AC IOP and CCI + attached lidocaine groups. A significant decrease in the number of Fos-like immunoreactive (LI) cells was observed in the CCI + lidocaine AC IOP group compared with that in the CCI group. These findings suggest that the effect of CCI + lidocaine AC IOP group may be caused by active permeation of lidocaine into the facial skin and electrical stimulation of the trigeminal nucleus.

Differential modulation of disynaptic cutaneous inhibition and excitation in ankle flexor motoneurons during fictive locomotion

1996 ◽  
Vol 76 (5) ◽  
pp. 2972-2985 ◽  
Author(s):  
A. M. Degtyarenko ◽  
E. S. Simon ◽  
R. E. Burke
Keyword(s):  
Electrical Stimulation ◽  
Dorsal Surface ◽  
Extension Phase ◽  
Fictive Locomotion ◽  
Plantar Surface ◽  
Cutaneous Reflex ◽  
Adult Cats ◽  
Differential Control ◽  
Almost All ◽  
Stimulation Of

1. Intracellular recording from extensor digitorum longus (EDL) and tibialis anterior (TA) alpha-motoneurons during fictive locomotion was used to examine patterns of modulation of oligosynaptic postsynaptic potentials (PSPs) produced by electrical stimulation of the cutaneous superficial peroneal (SP) and medial plantar (MPL) nerves in unanesthetized, decerebrate adult cats. 2. In all 20 EDL motoneurons studied, electrical stimulation of the SP nerve with single pulses at about twice threshold for the most excitable fibers in the nerve (2xT) produced either no synaptic potentials or relatively small oligosynaptic excitatory or inhibitory PSPs (EPSPs or IPSPs), both at rest and during the extension phase of fictive stepping. However, at the onset of the flexion phase large, presumably disynaptic IPSPs (central latencies 1.7–2.0 ms) appeared in the SP responses. These IPSPs usually decreased in amplitude later in the flexion phase despite maintained membrane depolarization. 3. In most (7/8) TA motoneurons, SP stimulation produced oligosynaptic EPSPs at rest and during the extension phase of fictive stepping. These EPSPs were suppressed during flexion in a majority of TA cells studied (5/8) but no clearly disynaptic IPSPs were found in any TA motoneuron. 4. In most EDL and TA motoneurons, stimulation of the MPL nerve produced oligosynaptic EPSPs at rest and during the extension phase, most with latencies in the presumably disynaptic range (< or = 2.0 ms). When present, these MPL EPSPs were suppressed throughout the flexion phase of stepping in almost all EDL (18/ 20) and TA (6/8) motoneurons examined. 5. The available evidence suggests that these modulation effects during fictive stepping are due primarily to convergence of control information from the spinal central pattern generator (CPG) for locomotion onto segmental interneurons in the oligosynaptic cutaneous pathways. 6. These observations extend the evidence for precise differential control of transmission through cutaneous reflex pathways in the cat hindlimb by the locomotor CPG. Taken together with earlier evidence about locomotor modulation of cutaneous PSPs in flexor digitorum longus (FDL) motoneurons, the data suggest that cutaneous information from the dorsal surface of the foot, carried in part by the SP nerve, projects to digit motoneurons (FDL and EDL) through discrete sets of last-order interneurons that also receive powerful excitation from the locomotor CPG during flexion. In contrast, the last-order interneurons that convey excitatory information from the SP nerve to at least some TA motoneurons are inhibited by the CPG during flexion. 7. Another contrast resides in the fact that oligosynaptic cutaneous excitation from the plantar surface of the foot, via the MPL nerve, is suppressed in FDL, EDL, and TA motoneurons during the flexion phase of locomotion. The available information is consistent with the possibility that MPL effects may be delivered to these motor nuclei by common interneurons. 8. We suggest an interneuronal circuitry that could account for these observations and discuss possible functional implications of modulation of these sensory pathways during locomotion.

scholarly journals Verification of neuroprotective effects of alpha-lipoic acid on chronic neuropathic pain in a chronic constriction injury rat model

2021 ◽  
Vol 16 (1) ◽  
pp. 222-228
Author(s):  
Junhao Wang ◽  
Zhaohui Lou ◽  
Haiyang Xi ◽  
Zhi Li ◽  
Lepeng Li ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Lipoic Acid ◽  
Rat Model ◽  
Chronic Constriction Injury ◽  
Neuroprotective Effect ◽  
Alpha Lipoic Acid ◽  
Chronic Neuropathic Pain ◽  
Neuroprotective Effects ◽  
Satellite Glial Cells ◽  
Withdrawal Threshold

Abstract Treatment of neuropathic pain is far from satisfactory. This study sought evidence of a neuroprotective effect of alpha-lipoic acid (ALA) to treat neuropathic pain in a chronic constriction injury (CCI) rat model. A total of 48 rats were randomly divided into sham, CCI, or CCI + ALA groups. Mechanical and thermal nociceptive thresholds were evaluated as behavioral assessments. Dorsal root ganglia cells were assessed morphologically with hematoxylin and eosin staining and for apoptosis with P53 immunohistochemical staining. Compared with the sham group, the CCI group had a shorter paw withdrawal threshold and paw withdrawal latency, abnormal morphologic manifestations, and increased numbers of satellite glial cells and P53+ cells. These changes were significantly reversed by treatment with ALA. Our study indicates neuroprotective effects of ALA on chronic neuropathic pain in a CCI rat model. ALA is potentially considered to be developed as a treatment for neuropathic pain caused by peripheral nerve injury, which requires further verification.

scholarly journals Peripherally Administered Botulinum Toxin Type A Localizes Bilaterally in Trigeminal Ganglia of Animal Model

Toxins ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 704
Author(s):  
Arief Waskitho ◽  
Yumiko Yamamoto ◽  
Swarnalakshmi Raman ◽  
Fumiya Kano ◽  
Huijiao Yan ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Botulinum Toxin ◽  
Mechanical Stimulation ◽  
Neurotransmitter Release ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Trigeminal Ganglia ◽  
Withdrawal Threshold ◽  
Orofacial Region

Peripheral nerve injury leads to sensory ganglion hyperexcitation, which increases neurotransmitter release and neuropathic pain. Botulinum toxin type A (BoNT/A) regulates pain transmission by reducing neurotransmitter release, thereby attenuating neuropathic pain. Despite multiple studies on the use of BoNT/A for managing neuropathic pain in the orofacial region, its exact mechanism of transport remains unclear. In this study, we investigated the effects of BoNT/A in managing neuropathic pain in two different animal models and its transport mechanism in the trigeminal nerve. Intraperitoneal administration of cisplatin induced bilateral neuropathic pain in the orofacial region, reducing the head withdrawal threshold to mechanical stimulation. Unilateral infraorbital nerve constriction (IONC) also reduced the ipsilateral head withdrawal threshold to mechanical stimulation. Unilateral peripheral administration of BoNT/A to the rat whisker pad attenuated cisplatin-induced pain behavior bilaterally. Furthermore, contralateral peripheral administration of BoNT/A attenuated neuropathy-induced behavior caused by IONC. We also noted the presence of BoNT/A in the blood using the mouse bioassay. In addition, the Alexa Fluor-488-labeled C-terminal half of the heavy chain of BoNT/A (BoNT/A-Hc) was localized in the neurons of the bilateral trigeminal ganglia following its unilateral administration. These findings suggest that axonal and hematogenous transport are involved in the therapeutic effects of peripherally administered BoNT/A in the orofacial region.

scholarly journals Vitexin alleviates neuropathic pain in a mouse chronic constriction injury model by inactivation of NF-κB

2020 ◽  
Vol 19 (5) ◽  
pp. 989-994
Author(s):  
Wentong Xu ◽  
Xueli Zhu ◽  
Gonghao Zhan ◽  
Liangyu Sheng ◽  
Yanwei Chen
Keyword(s):  
Neuropathic Pain ◽  
Inflammatory Cytokines ◽  
Chronic Constriction Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Mechanical Hypersensitivity ◽  
Withdrawal Threshold ◽  
Before And After ◽  
Cci Model ◽  
Pro Inflammatory Cytokines

Purpose: To investigate the therapeutic effect of vitexin on neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI).Methods: The CCI model was established by four chronic ligatures in the sciatic nerve. Vitexin was intraperitoneally administered (10 mg/kg, once daily) for 21 days. Mechanical withdrawal threshold (MWT) and paw withdrawal latency (PWL) were determined before and after the establishment of CCI model. The spinal cords were collected to measure mRNA levels by reverse-transcriptase polymerase chain reaction (RT-PCR) enzyme-linked immunosorbent assay (ELISA). Western blot was used to examine protein expression levels.Results: Vitexin reversed the CCI-induced reduction in MWT and PWL values, indicating that it lowered mechanical hypersensitivity response and hyperalgesia caused thermal stimulation (p < 0.05). The elevated levels of IL-6, IL-1β, and TNFα observed in CCI-treated mice were also inhibited by vitexin, suggesting that it suppressed pro-inflammatory cytokines. Moreover, vitexin attenuated CCI-induced activation of NF-κB signaling in CCI-treated mice (p < 0.05).Conclusion: Vitexin alleviates NP by inhibiting pro-inflammatory cytokines and NF-κB signaling in CCItreated mice. Thus, it is a potential target for NP treatment. Keywords: Vitexin, Neuropathic pain, Chronic constriction injury, Mechanical hypersensitivity, Hyperalgesia, NF-κB

scholarly journals Electroacupuncture suppresses glucose metabolism and GLUT-3 expression in medial prefrontal cortical in rats with neuropathic pain

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Menghong Jiang ◽  
Xiaomei Chen ◽  
Liangping Zhang ◽  
Weiting Liu ◽  
Xiangmei Yu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Glucose Metabolism ◽  
Sham Group ◽  
Glucose Transporter ◽  
Thermal Hyperalgesia ◽  
Withdrawal Threshold ◽  
Prefrontal Cortical ◽  
Positron Emission ◽  
Immune Histochemistry ◽  
The Right

Abstract Background Accumulating evidence has demonstrated that the electroacupuncture (EA) stimulation could effectively alleviate neuropathic pain. The medial prefrontal cortex (mPFC) is a vital part of the cortical representation of pain in the brain, and its glucose metabolism is mostly affected in the progression of pain. However, the central mechanism of EA analgesia remains unclear. Methods Fifty-four male SD rats were equally randomized into sham surgery (Sham) group, chronic constriction injury (CCI) group and EA stimulation (EA) group. The CCI model, involving ligature of the right sciatic nerve, was established in all animals except the Sham group. EA stimulation was applied on the right side acupoints of Huantiao (GB30) and Yanglingquan (GB34) in the EA group. Paw withdrawal threshold (PWT) and paw thermal withdrawal latency (PWL) were measured. The 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) was used to evaluate glucose metabolism changes in the mPFC. The expression of glucose transporter 3 (GLUT-3) in the mPFC was determined by immune histochemistry and ELISA. Results Comparing with CCI groups, EA treatment was obviously reversed CCI-induced mechanical allodynia (P < 0.01), thermal hyperalgesia (P < 0.01) and the increase of glucose metabolism in the left mPFC (P < 0.05). Furthermore, EA treatment significantly decreased the protein expression of GLUT-3 in the left mPFC (P < 0.01). Conclusions Our results indicate that EA analgesia effect may be related to suppressing the glucose metabolism and GLUT-3 expression in the mPFC. This study could provide a potential insight into the central mechanisms involved in the analgesic effect of EA.

scholarly journals Antiallodynic Effect of Herbal Medicine Yokukansan on Peripheral Neuropathy in Rats with Chronic Constriction Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Yasuyuki Suzuki ◽  
Hiromasa Mitsuhata ◽  
Mitsutoshi Yuzurihara ◽  
Yoshio Kase
Keyword(s):  
Neuropathic Pain ◽  
Chronic Constriction Injury ◽  
Glutamate Transporter ◽  
Herbal Medicines ◽  
Tricyclic Antidepressant ◽  
Glutamatergic Neurotransmission ◽  
Cold Allodynia ◽  
Pain Symptoms ◽  
Antiallodynic Effect ◽  
Stimulation Of

Yokukansan, one of the traditional Japanese herbal medicines, ameliorated neuropathic pain symptoms in patients. In this study, we investigated the effects of yokukansan on neuropathic pain in chronic constriction injury (CCI) model. Oral administration of yokukansan significantly inhibited mechanical and cold allodynia in the von Frey hair or acetone test, respectively. In comparison, amitriptyline, a tricyclic antidepressant, demonstrated moderate, but not significant, antiallodynic effects in the mechanical and cold tests. Yokukansan significantly inhibited the cerebrospinal fluid dialysate level of glutamate that had increased by the stimulation of brush or acetone. Glutamate transporter inhibitors, DL-threo-beta-hydroxy aspartate and dihydrokainate, decreased the yokukansan-induced antiallodynic actions in CCI rats. Our results suggest that yokukansan was confirmed to have antiallodynic effects in CCI rats, which are related to a blockade of glutamatergic neurotransmission via activation of glutamate transporters in the spinal cord.

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