C‐X‐C motif chemokine ligand 1 and its receptor C‐X‐C motif chemokine receptor 2 in trigeminal ganglion contribute to nerve injury‐induced orofacial mechanical allodynia

2021 ◽  
Author(s):  
Jie Yang ◽  
Fei Liu ◽  
Yan‐Yan Zhang ◽  
Jiu Lin ◽  
Yue‐Ling Li ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Trigeminal Ganglion ◽  
Chemokine Receptor ◽  
Mechanical Allodynia ◽  
Chemokine Ligand

Pannexin 1 role in the trigeminal ganglion in infraorbital nerve injury‐induced mechanical allodynia

Oral Diseases ◽  
2022 ◽  
Author(s):  
Ryoko Kurisu ◽  
Tadashi Saigusa ◽  
Yuri Aono ◽  
Yoshinori Hayashi ◽  
Suzuro Hitomi ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Trigeminal Ganglion ◽  
Mechanical Allodynia ◽  
Infraorbital Nerve ◽  
Pannexin 1

scholarly journals P2.01-040 CXC Chemokine Receptor 3 and ELR Motif Negative CXC Chemokine Ligand Axis in Non-Small Cell Lung Cancer

2017 ◽  
Vol 12 (1) ◽  
pp. S809-S810
Author(s):  
Artjoms Spaks ◽  
Donats Breiva ◽  
Ilmars Tracums ◽  
Anastasija Bistrova ◽  
Krista Grigorovica ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Chemokine Receptor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cxc Chemokine ◽  
Chemokine Ligand

Blockade of microglial activation reduces mechanical allodynia in rats with compression of the trigeminal ganglion

2012 ◽  
Vol 36 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Seung R. Han ◽  
Gwi Y. Yang ◽  
Myung H. Ahn ◽  
Min J. Kim ◽  
Jin S. Ju ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Mechanical Allodynia ◽  
Microglial Activation

scholarly journals Macrophages in trigeminal ganglion contribute to ectopic mechanical hypersensitivity following inferior alveolar nerve injury in rats

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Dulguun Batbold ◽  
Masamichi Shinoda ◽  
Kuniya Honda ◽  
Akihiko Furukawa ◽  
Momoko Koizumi ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Trigeminal Ganglion ◽  
Inferior Alveolar Nerve ◽  
Mechanical Hypersensitivity ◽  
Inferior Alveolar Nerve Injury

scholarly journals Plasticity-Related PKMζSignaling in the Insular Cortex Is Involved in the Modulation of Neuropathic Pain after Nerve Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jeongsoo Han ◽  
Minjee Kwon ◽  
Myeounghoon Cha ◽  
Motomasa Tanioka ◽  
Seong-Karp Hong ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Nerve Injury ◽  
Neural Plasticity ◽  
Mechanical Allodynia ◽  
Insular Cortex ◽  
Long Term Potentiation ◽  
Inhibitory Peptide ◽  
Term Potentiation ◽  
Potential Applications

The insular cortex (IC) is associated with important functions linked with pain and emotions. According to recent reports, neural plasticity in the brain including the IC can be induced by nerve injury and may contribute to chronic pain. Continuous active kinase, protein kinase Mζ(PKMζ), has been known to maintain the long-term potentiation. This study was conducted to determine the role of PKMζin the IC, which may be involved in the modulation of neuropathic pain. Mechanical allodynia test and immunohistochemistry (IHC) of zif268, an activity-dependent transcription factor required for neuronal plasticity, were performed after nerve injury. Afterζ-pseudosubstrate inhibitory peptide (ZIP, a selective inhibitor of PKMζ) injection, mechanical allodynia test and immunoblotting of PKMζ, phospho-PKMζ(p-PKMζ), and GluR1 and GluR2 were observed. IHC demonstrated that zif268 expression significantly increased in the IC after nerve injury. Mechanical allodynia was significantly decreased by ZIP microinjection into the IC. The analgesic effect lasted for 12 hours. Moreover, the levels of GluR1, GluR2, and p-PKMζwere decreased after ZIP microinjection. These results suggest that peripheral nerve injury induces neural plasticity related to PKMζand that ZIP has potential applications for relieving chronic pain.

Sortilins in neuropathic pain

2012 ◽  
Vol 3 (3) ◽  
pp. 183-184
Author(s):  
M. Richner ◽  
O.J. Bjerrum ◽  
Y. De Koninck ◽  
A. Nykjaer ◽  
C.B. Vaegter
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Mechanical Allodynia ◽  
Molecular Mechanisms ◽  
Intrathecal Injection ◽  
Ion Concentration ◽  
Down Regulation

AbstractBackground/aimsThe molecular mechanisms underlying neuropathic pain are incompletely understood, but recent data suggest that down-regulation of the chloride extruding co-transporter KCC2 in spinal cord sensory neurons is critical: Following peripheral nerve injury, activated microglia in the spinal cord release BDNF, which stimulates neuronal TrkB receptors and ultimately results in the reduction of KCC2 levels. Consequently, neuronal intracellular chloride ion concentration increases, impairing GABAA-receptor mediated inhibition. We have previously described how the receptor sortilin modulates neurotrophin signaling by facilitating anterograde transport of Trk receptors. Unpublished data further link SorCS2, another member of the Sortilins family of sorting receptors (sortilin, SorLA and SorCS1–3) to BDNF signaling by regulating presynaptic TrkB trafficking. The purpose of this study is to explore the involvement of Sortilins in neuropathic pain.MethodsWe subjected wild-type (wt), sortilin knockout (Sort1-/-) and SorCS2 knockout (SorCS2-/-) mice to the Spared Nerve Injury (SNI) model of peripheral nerve injury. Mechanical allodynia was measured by von Frey filaments using the up-down-up method and a 3-out-of-5 thresshold.ResultsAs previously described by several groups, wt mice developed significant mechanical allodynia following SNI. Interestingly however, mice lacking sortilin or SorCS2 were fully protected from development of allodynia and did not display KCC2 down-regulation following injury. In addition, a single intrathecal injection of antibodies against sortilin or SorCS2 could delay or rescue mechanical allodynia in wt SNI mice for 2-3 days. Finally, neither sortilin nor SorCS2 deficient mice responded to intrathecal injection of BDNF, in contrast to wt mice which developed transient mechanical allodynia.ConclusionWe hypothesize that sortilin and SorCS2 are involved in neuropathic pain development by regulating TrkB signaling. Alternatively, Sortilins may directly influence the regulation of KCC2 membrane levels following injury. Both hypotheses are currently being investigated by our group.

Anion exchanger 3 in dorsal root ganglion contributes to nerve injury-induced chronic mechanical allodynia and thermal hyperalgesia

2018 ◽  
Vol 70 (3) ◽  
pp. 374-382 ◽  
Author(s):  
Marian J. Pérez-Rodríguez ◽  
Isabel Velazquez-Lagunas ◽  
Alejandro Pluma-Pluma ◽  
Paulino Barragán-Iglesias ◽  
Vinicio Granados-Soto
Keyword(s):  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Anion Exchanger ◽  
Dorsal Root ◽  
Mechanical Allodynia ◽  
Thermal Hyperalgesia
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