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AKAP150 involved in paclitaxel-induced neuropathic pain via inhibiting CN/NFAT2 pathway and downregulating IL-4
In this study, we found that A-kinase anchor protein 150 (AKAP150) was significantly upregulated after paclitaxel injection. Inhibition of AKAP150 via siRNA or AKAP150flox/flox in rodents alleviated the pain behavior induced by paclitaxel, and partly restored the decreased calcineurin (CN) phosphatase activity after paclitaxel treatment. Paclitaxel decreased the expression of anti-inflammatory cytokine interleukin-4 (IL-4), and intrathecal injections of IL-4 effectively alleviated paclitaxel-induced hypersensitivity and the frequency of dorsal root ganglion (DRG) neurons action potential. The decreased CN enzyme activity, ...
Source: Brain, Behavior, and Immunity - January 11, 2018 Category: Neurology Source Type: research

AKAP150 involved in Paclitaxel-Induced Neuropathic Pain via Inhibiting CN/NFAT2 pathway and downregulating IL-4.
In this study, we found that A-kinase anchor protein 150 (AKAP150) was significantly upregulated after paclitaxel injection. Inhibition of AKAP150 via siRNA or AKAP150(flox/flox) in rodents alleviated the pain behavior induced by paclitaxel, and partly restored the decreased calcineurin (CN) phosphatase activity after paclitaxel treatment. Paclitaxel decreased the expression of anti-inflammatory cytokine interleukin-4 (IL-4), and intrathecal injections of IL-4 effectively alleviated paclitaxel-induced hypersensitivity and the frequency of dorsal root ganglion (DRG) neurons action potential. The decreased CN enzyme activity...
Source: Brain, Behavior, and Immunity - October 19, 2017 Category: Neurology Authors: Nie B, Liu C, Bai X, Chen X, Wu S, Zhang S, Huang Z, Xie M, Xu T, Xin W, Zeng W, Ouyang H Tags: Brain Behav Immun Source Type: research

Toll-Like Receptor-4/p38 MAPK Signaling in the Dorsal Horn Contributes to P2X4 Receptor Activation and BDNF Over-secretion In Cancer Induced Bone Pain
In this study, we focused on whether TLR4- mitogen-activated protein kinases, p38 (p38 MAPK) contributes to P2X4R activation and brain-derived neurotrophic factor (BDNF) over-secretion in CIBP. In in vitro experiment, the results showed that BDNF expression evoked by ATP stimulation was dependent on TLR4-p38. In in vivo experiment, the results demonstrated that an intrathecal injection of TLR4 siRNA alleviated nociception induced by lipopolysaccharide (LPS) plus ATP or CIBP with decreased expression of P2X4R, TLR4, BDNF, interleukin-6 (IL-6) and phosphorylated-p38 MAPK (p-p38 MAPK). Moreover, injection with p38MAPK inhibit...
Source: Neuroscience Research - June 29, 2017 Category: Neuroscience Source Type: research

CREB-regulated transcription coactivator 1 enhances CREB-dependent gene expression in spinal cord to maintain the bone cancer pain in mice
Conclusions Upregulation of CRTC1 enhancing CREB-dependent gene transcription in spinal cord may play an important role in bone cancer pain. Inhibition of spinal CRTC1 expression reduced bone cancer pain. Interruption to the positive feedback circuit between CREB/CRTC1 and its targets may contribute to the analgesic effects. These findings may provide further insight into the mechanisms and treatment of bone cancer pain.
Source: Molecular Pain - April 7, 2016 Category: Molecular Biology Authors: Liang, Y., Liu, Y., Hou, B., Zhang, W., Liu, M., Sun, Y.-E., Ma, Z., Gu, X. Tags: Research Article Source Type: research

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice
Publication date: Available online 24 June 2015 Source:Brain, Behavior, and Immunity Author(s): Norimitsu Morioka , Fang Fang Zhang , Yoki Nakamura , Tomoya Kitamura , Kazue Hisaoka-Nakashima , Yoshihiro Nakata Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes, not neurons or microglia, in the spinal dorsal horn. Hind paw mechanical hypersensitivity was observed beginning 3days ...
Source: Brain, Behavior, and Immunity - July 3, 2015 Category: Neurology Source Type: research

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice.
Abstract Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes, not neurons or microglia, in the spinal dorsal horn. Hind paw mechanical hypersensitivity was observed beginning 3 days after partial sciatic nerve ligation (PSNL), but a persistent downregulation of astrocytic Cx43 in ipsilateral lumbar spinal dorsal horn was not observed until 7 days post-PSNL, suggesting that ...
Source: Brain, Behavior, and Immunity - June 23, 2015 Category: Neurology Authors: Morioka N, Zhang FF, Nakamura Y, Kitamura T, Hisaoka-Nakashima K, Nakata Y Tags: Brain Behav Immun Source Type: research

Role of ATP-sensitive potassium channels in modulating nociception in rat model of bone cancer pain.
Abstract Bone cancer pain is a major clinical problem and remains difficult to treat. ATP-sensitive potassium (KATP) channels may be involved in regulating nociceptive transmission at the spinal cord level. We determined the role of spinal KATP channels in the control of mechanical hypersensitivity in a rat model of bone cancer pain. The rat model of bone cancer pain was induced by implanting rat mammary gland carcinoma cells (Walker256) into the tibias. KATP modulators (pinacidil and glibenclamide) or the specific Kir6.2-siRNA were injected via an intrathecal catheter. The mechanical withdrawal threshold of rats ...
Source: Brain Research - January 27, 2014 Category: Neurology Authors: Xia H, Zhang D, Yang S, Wang Y, Xu L, Wu J, Ren J, Yao W, Fan L, Zhang C, Tian Y, Pan HL, Wang X Tags: Brain Res Source Type: research

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