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Molecular Pain

Zhen Liu, Fan Liu, Xiaowen Liu, Chao Ma, Jing Zhao
Surgical incision-induced nociception contributes to the occurrence of postoperative cognitive dysfunction (POCD). However, the exact mechanisms involved remain unclear. Brain-derived neurotrophic factor (BDNF) has been demonstrated to improve fear learning ability. Additionally, BDNF expression is influenced by the peripheral nociceptive stimulation. Therefore, we hypothesized that surgical incision-induced nociception may cause learning impairment by inhibiting the BDNF/TrkB signaling pathway. The fear conditioning test, ELISA and Western blot analyses were used to confirm our hypothesis and determine the effect of a plantar incision on the fear learning and the BDNF/TrkB signaling pathway in the hippocampus and amygdala...
September 20, 2018: Molecular Pain
Guangchen Ji, Vadim Yakhnitsa, Takaki Kiritoshi, Peyton Presto, Volker Neugebauer
The amygdala plays a key role in fear learning and extinction and has emerged as an important node of emotional-affective aspects of pain and pain modulation. Impaired fear extinction learning, which involves prefrontal cortical control of amygdala processing, has been linked to neuropsychiatric disorders. Here we tested the hypothesis that fear extinction learning ability can predict the magnitude of neuropathic pain. We correlated fear extinction (FE) learning in naive adult male rats with sensory and affective behavioral outcome measures (mechanical thresholds, vocalizations, anxiety- and depression-like behaviors) before and after induction of the spinal nerve ligation (SNL) model of neuropathic pain compared to sham controls...
September 13, 2018: Molecular Pain
Nozomu Okamoto, Masayo Okumura, Osamu Tadokoro, Norio Sogawa, Mihoko Tomida, Eiji Kondo
Transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel that is expressed in the sensory neurons and responds to various noxious stimuli including heat and capsaicin. The molecular property of TRPV1 have been clearly examined, however, there are obvious individual differences in human sensitivity to thermal stimuli and capsaicin. Here, we examined the possibility that different genome sequence of human TRPV1 caused the different sensitivity to heat or capsaicin. The sensitivities to burning pain and capsaicin of Japanese adult subjects were compared with their TRPV1 genome sequence, and we detected 6 SNPs, and 11 SNPs related to burning pain and capsaicin sensitivity, respectively...
September 13, 2018: Molecular Pain
Pengtao Li, Quan Zhang, Zhi Xiao, Shouyang Yu, Yan Yan, Ying Qin
Cancer pain is a well-known serious complication in metastatic or terminal cancer patients. Current pain management remains unsatisfactory. The activation of spinal and supraspinal P2X7 receptors plays a crucial role in the induction and maintenance mechanisms of various kinds of acute or chronic pain. The midbrain periaqueductal gray (PAG) is a vital supraspinal site of the endogenous descending pain-modulating system. Tramadol is a synthetic, centrally acting analgesic agent that exhibits considerable efficacy in clinically relieving pain...
September 10, 2018: Molecular Pain
Ieva Satkeviciute, Andrew Dilley
Many patients with neuropathic pain present without signs of nerve injury on routine clinical examination. Some of these patients may have inflamed peripheral nerves (neuritis). In this study, we have examined whether neuritis causes changes within the dorsal horn that may contribute to a central pain mechanism. Comparisons have been made to a model of axonal transport disruption induced using vinblastine, since neuritis disrupts such processes. At the peak of cutaneous hypersensitivities, recordings from wide dynamic range (WDR) neurons revealed increases in wind-up following neuritis but not vinblastine treatment...
August 21, 2018: Molecular Pain
Qi-Yu Chen, Tao Chen, Li-Jun Zhou, Xian-Guo Liu, Min Zhuo
Spinal nociceptive transmission receives biphasic modulation from supraspinal structures. Recent studies demonstrate that the anterior cingulate cortex (ACC) facilitates spinal excitatory synaptic transmission and nociceptive reflex. However, whether the top-down descending facilitation can cause long-term synaptic changes in spinal cord remains unclear. In the present study, we recorded C-fiber evoked field potentials in spinal dorsal horn and found that the ACC stimulation caused enhancement of C fiber mediated responses...
August 14, 2018: Molecular Pain
Man-Xiu Xie, He-Quan Zhu, Rui-Ping Pang, Bing-Ting Wen, Xian-Guo Liu
Bulleyaconitine A, a diterpenoid alkaloid isolated from Aconitum bulleyanum plants, has been used for the treatment of chronic pain in China since 1985. Clinical studies show that the oral administration of bulleyaconitine A is effective for treating different kinds of chronic pain, including back pain, joint pain, and neuropathic pain with minimal side effect in human patients. The experimental studies have revealed that bulleyaconitine A at therapeutic doses potently inhibits the peripheral sensitization and central sensitization that underlie chronic pain and has no effect on acute pain...
January 2018: Molecular Pain
Robert J Danaher, Liping Zhang, Connor J Donley, Nashwin A Laungani, S Elise Hui, Craig S Miller, Karin N Westlund
Chronic orofacial pain is a significant health problem requiring identification of regulating processes. Involvement of epigenetic modifications that is reported for hindlimb neuropathic pain experimental models, however, is less well studied in cranial nerve pain models. Three independent observations reported here are the (1) epigenetic profile in mouse trigeminal ganglia (TG) after trigeminal inflammatory compression (TIC) nerve injury mouse model determined by gene expression microarray, (2) H3K9 acetylation pattern in TG by immunohistochemistry, and (3) efficacy of histone deacetylase (HDAC) inhibitors to attenuate development of hypersensitivity...
January 2018: Molecular Pain
Wan-Hung Lee, Lawrence M Carey, Li-Li Li, Zhili Xu, Yvonne Y Lai, Michael J Courtney, Andrea G Hohmann
Elevated N-methyl-D-aspartate receptor activity contributes to central sensitization. Our laboratories and others recently reported that disrupting protein-protein interactions downstream of N-methyl-D-aspartate receptors suppresses pain. Specifically, disrupting binding between the enzyme neuronal nitric oxide synthase and either its upstream (postsynaptic density 95 kDa, PSD95) or downstream (e.g. nitric oxide synthase 1 adaptor protein, NOS1AP) protein partners suppressed inflammatory and/or neuropathic pain...
January 2018: Molecular Pain
Hitoshi Uchida, Shinji Matsumura, Tayo Katano, Masahiko Watanabe, Jens Schlossmann, Seiji Ito
cGMP-dependent kinase-I (cGKI) is known to regulate spinal pain processing. This enzyme consists of two isoforms (cGKIα and cGKIβ) that show distinct substrate specificity and tissue distribution. It has long been believed that the α isoform is exclusively expressed in the adult dorsal root ganglion. The aim of the present study was to reexamine the expression of cGKI isoforms in the adult mouse dorsal root ganglion using isoform-specific cGKI antibodies whose specificities had been validated in the previous studies...
January 2018: Molecular Pain
Liang Zhao, Dan Li, Nan Liu, Lu Liu, Zhuo Zhang, Chao Gao, Hitoshi Kawano, Fang-Yuan Zhou, Hong-Peng Li
Extracellular regulated protein kinase (ERK) pathway activation in astrocytes and neurons has been reported to be critical for neuropathic pain development after chronic constriction injury. TGN-020 was found to be the most potent aquaporin 4 inhibitor among the agents studied. The present study aimed to assess whether the inhibition of aquaporin 4 had an analgesic effect on neuropathic pain and whether the inhibition of astrocytic activation and ERK pathway was involved in the analgesic effect of TGN-020. We thus found that TGN-020 upregulated the threshold of thermal and mechanical allodynia, downregulated the expression of interleukin-1β, interleukin-6, and tumor necrosis factor-α, attenuated the astrocytic activation and suppressed the activation of mitogen-activated protein kinase pathways in the spinal dorsal horn and dorsal root ganglion...
January 2018: Molecular Pain
Chilman Bae, Jigong Wang, Hyun Soo Shim, Shao-Jun Tang, Jin Mo Chung, Jun-Ho La
Reactive oxygen species has been suggested as a key player in neuropathic pain, causing central sensitization by changing synaptic strengths in spinal dorsal horn neurons. However, it remains unclear as to what type of reactive oxygen species changes what aspect of synaptic strengths for central sensitization in neuropathic pain conditions. In this study, we investigated whether mitochondrial superoxide affects both excitatory and inhibitory synaptic strengths in spinal dorsal horn neurons after peripheral nerve injury...
January 2018: Molecular Pain
Malik Bechakra, Mariska D Nieuwenhoff, Joost van Rosmalen, Geert Jan Groeneveld, Marjan Scheltens-de Boer, Pieter Sonneveld, Pieter A van Doorn, Chris I de Zeeuw, Joost Lm Jongen
Bortezomib is a mainstay of therapy for multiple myeloma, frequently complicated by painful neuropathy. The objective of this study was to describe clinical, electrophysiological, and pathological changes of bortezomib-induced peripheral neuropathy (BiPN) in detail and to correlate pathological changes with pain descriptors. Clinical data, nerve conduction studies, and lower leg skin biopsies were collected from 22 BiPN patients. Skin sections were immunostained using anti-protein gene product 9.5 (PGP9.5) and calcitonin gene-related peptide (CGRP) antibodies...
January 2018: Molecular Pain
Chaoyang Liu, Yixin Zhang, Qing Liu, Li Jiang, Maolin Li, Sha Wang, Ting Long, Wei He, Xueying Kong, Guangcheng Qin, Lixue Chen, Yuhong Zhang, Jiying Zhou
Objective Previous studies of neuropathic pain have suggested that the P2X4 purinoceptor (P2X4R) in spinal microglia is essential for maintaining allodynia following nerve injury. However, little is known about its role in inflammatory soup-induced trigeminal allodynia, which closely mimics chronic migraine status. Here, we determined the contributions of P2X4R and related signaling pathways in an inflammatory soup-induced trigeminal allodynia model. Methods P2X4R gene and protein levels in the trigeminal nucleus caudalis were analyzed following repeated dural inflammatory soup infusions...
January 2018: Molecular Pain
Rebecca Dalgarno, Heather Leduc-Pessah, Alexandra Pilapil, Charlie Ht Kwok, Tuan Trang
Pain hypersensitivity resulting from peripheral nerve injury depends on pathological microglial activation in the dorsal horn of the spinal cord. This microglial activity is critically modulated by P2X7 receptors (P2X7R) and ATP stimulation of these receptors produces mechanical allodynia, a defining feature of neuropathic pain. Peripheral nerve injury increases P2X7R expression and potentiates its cation channel function in spinal microglia. Here, we report a means to preferentially block the potentiation of P2X7R function by delivering a membrane permeant small interfering peptide that targets Y382-384 , a putative tyrosine phosphorylation site within the P2X7R intracellular C-terminal domain...
January 2018: Molecular Pain
J David Clark, Vivianne L Tawfik, Maral Tajerian, Wade S Kingery
Complex regional pain syndrome (CRPS) is a highly enigmatic syndrome typically developing after injury or surgery to a limb. Severe pain and disability are common among those with chronic forms of this condition. Accumulating evidence suggests that CRPS may involve both autoinflammatory and autoimmune components. In this review article, evidence for dysfunction of both the innate and adaptive immune systems in CRPS is presented. Findings from human studies in which cytokines and other inflammatory mediators were measured in the skin of affected limbs are discussed...
January 2018: Molecular Pain
Xian Wang, Xiaofeng Shen, Yingli Xu, Shiqin Xu, Fan Xia, Bei Zhu, Yusheng Liu, Wei Wang, Haibo Wu, Fuzhou Wang
Neuropathic pain is a common chronic pain condition with mechanisms far clearly been elucidated. Mounting preclinical and clinical studies have shown neuropathic pain is highly associated with histone acetylation modification, which follows expression regulation of various pain-related molecules such as mGluR1/5, glutamate aspartate transporter, glutamate transporter-1, GAD65, Nav 1.8, Kv4.3, μ-opioid receptor, brain-derived neurotrophic factor, and certain chemokines. As two types of pivotal enzymes involved in histone acetylation, histone deacetylases induce histone deacetylation to silence gene expression; in contrast, histone acetyl transferases facilitate histone acetylation to potentiate gene transcription...
January 2018: Molecular Pain
Shu-Ping Chen, Jia Sun, Ya-Qun Zhou, Fei Cao, Cody Braun, Fang Luo, Da-Wei Ye, Yu-Ke Tian
Cancer-induced bone pain is one of the most severe types of pathological pain, which often occurs in patients with advanced prostate, breast, and lung cancer. It is of great significance to improve the therapies of cancer-induced bone pain due to the opioids' side effects including addiction, sedation, pruritus, and vomiting. Sinomenine, a traditional Chinese medicine, showed obvious analgesic effects on a rat model of chronic inflammatory pain, but has never been proven to treat cancer-induced bone pain. In the present study, we investigated the analgesic effect of sinomenine after tumor cell implantation and specific cellular mechanisms in cancer-induced bone pain...
January 2018: Molecular Pain
Ting Yu, Lei Li, Huaxiang Liu, Hao Li, Zhen Liu, Zhenzhong Li
Background Diabetic neuropathic pain is poorly controlled by analgesics, and the precise molecular mechanisms underlying hyperalgesia remain unclear. The KCNQ2/3/5 channels expressed in dorsal root ganglion neurons are important in pain transmission. The expression and activity of KCNQ2/3/5 channels in dorsal root ganglion neurons in rats with diabetic neuropathic pain were investigated in this study. Methods The mRNA levels of KCNQ2/3/5 channels were analyzed by real-time polymerase chain reaction. The protein levels of KCNQ2/3/5 channels were evaluated by Western blot assay...
January 2018: Molecular Pain
Haruka Hiyama, Yuichi Yano, Kanako So, Satoshi Imai, Kazuki Nagayasu, Hisashi Shirakawa, Takayuki Nakagawa, Shuji Kaneko
Background Diabetic peripheral neuropathy is a common long-term complication of diabetes. Accumulating evidence suggests that vascular impairment plays important roles in the pathogenesis of diabetic peripheral neuropathy, while the mechanism remains unclear. We recently reported that transient receptor potential ankyrin 1 (TRPA1) is sensitized by hypoxia, which can contribute to cold hypersensitivity. In this study, we investigated the involvement of TRPA1 and vascular impairment in painful diabetic peripheral neuropathy using streptozotocin-induced diabetic model mice...
January 2018: Molecular Pain
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