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| 1 | Sex-Dependent Glial Signaling in Pathological Pain:Distinct Roles of Spinal Microglia and Astrocytes显示文摘Increasing evidence suggests that spinal microglia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain following intrathecal injection in male and female mice. These modulators were the microglial inhibitors minocycline and ZVEID(a caspase-6 inhibitor) and the astroglial inhibitors L-α-aminoadipate(L-AA, an astroglial toxin) and carbenoxolone(a connexin 43 inhibitor), as well as U0126(an ERK kinase inhibitor) and D-JNKI-1(a c-Jun N-terminal kinase inhibitor). We found that spinal administration of minocycline or ZVEID, or Caspase6 deletion, reduced formalin-induced inflammatory and nerve injury-induced neuropathic pain primarily in male mice. In contrast,intrathecal L-AA reduced neuropathic pain but not inflammatory pain in both sexes. Intrathecal U0126 and D-JNKI-1 reduced neuropathic pain in both sexes. Nerve injury caused spinal upregulation of the astroglial markers GFAP and Connexin 43 in both sexes. Collectively, our data confirmed male-dominant microglial signaling but also revealed sex-independent astroglial signaling in the spinal cord in inflammatory and neuropathic pain. | Gang Chen Xin Luo M.Yawar Qadri Temugin Berta Ru-Rong Ji | 2018 | Neuroscience Bulletin2018，34，1： | 18 |
| 2 | Expression and Role of Voltage-Gated Sodium Channels in Human Dorsal Root Ganglion Neurons with Special Focus on Nav1.7,Species Differences, and Regulation by Paclitaxel显示文摘Voltage-gated sodium channels(Navs) play an important role in human pain sensation. However, the expression and role of Nav subtypes in native human sensory neurons are unclear. To address this issue, we obtained human dorsal root ganglion(hDRG) tissues from healthy donors. PCR analysis of seven DRG-expressed Nav subtypes revealed that the hDRG has higher expression of Nav1.7(~50% of total Nav expression) and lower expression of Nav1.8(~12%), whereas the mouse DRG has higher expression of Nav1.8(~45%) and lower expression of Nav1.7(~18%). To mimic Nav regulation in chronic pain, we treated hDRG neurons in primary cultures with paclitaxel(0.1-1 μmol/L) for 24 h. Paclitaxel increased the Nav 1.7 but not Nav1.8 expression and also increased the transient Na^+ currents and action potential firing frequency in small-diameter(<50 μm) hDRG neurons. Thus, the hDRG provides a translational model in which to study'human pain in a dish' and test new pain therapeutics. | Wonseok Chang Temugin Berta Yong Ho Kim Sanghoon Lee Seok-Yong Lee Ru-Rong Ji | 2018 | Neuroscience Bulletin2018，34，1： | 12 |
| 3 | Nociceptive neurons regulate innate and adaptive immunity and neuropathic pain through MyD88 adapter显示文摘 | Xing-Jun Liu Yanli Zhang Tong LIU Zhen-Zhong Xu Chul-Kyu Park Temugin Berta Dianhua Jiang Ru-Rong Ji | 2014 | Cell Research2014，24，11： | 5 |
| 4 | Microglia and spinal cord synaptic plasticity in persistent pain显示文摘 | Sarah Taves Temugin Berta Gang Chen | 2013 | Neural Plast2013，2013，75： | 1 |
| 5 | Transcriptional and functional profiles of voltage-gated Na + channels in injured and non-injured DRG neurons in the SNI model of neuropathic pain显示文摘 | Temugin Berta Olivier Poirot Marie Pertin Ru-Rong Ji Stephan Kellenberger Isabelle Decosterd | 2007 | Molecular and Cellular Neuroscience2007，，2： | 1 |
| 6 | The Antinociceptive Effect of Sympathetic Block is Mediated by Transforming Growth Factor β in a Mouse Model of Radiculopathy显示文摘Although sympathetic blockade is clinically used to treat pain,the underlying mechanisms remain unclear.We developed a localized microsympathectomy(mSYMPX),by cutting the grey rami entering the spinal nerves near the rodent lumbar dorsal root ganglia(DRG).In a chemotherapy-induced peripheral neuropathy model,mSYMPX attenuated pain behaviors via DRG macrophages and the anti-inflammatory actions of transforming growth factor-β(TGF-β)and its receptor TGF-βR1.Here,we examined the role of TGF-βin sympathetic-mediated radiculopathy produced by local inflammation of the DRG(LID).Mice showed mechanical hypersensitivity and transcriptional and protein upregulation of TGF-β1 and TGF-βR1 three days after LID.Microsympathectomy prevented mechanical hypersensitivity and further upregulated Tgfb1 and Tgfbr1.Intrathecal delivery of TGF-β1 rapidly relieved the LID-induced mechanical hypersensitivity,and TGF-βR1 antagonists rapidly unmasked the mechanical hypersensitivity after LID+mSYMPX.In situ hybridization showed that Tgfb1 was largely expressed in DRG macrophages,and Tgfbr1 in neurons.We suggest that TGF-βsignaling is a general underlying mechanism of local sympathetic blockade. | Debora Denardin Luckemeyer Wenrui Xie Arthur Silveira Prudente Katherine A.Qualls Raquel Tonello Judith A.Strong Temugin Berta Jun-Ming Zhang | 2023 | Neuroscience Bulletin2023，39，9： | 0 |
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