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

NGF Augmentation rescues trigeminal ganglion and principalis neurons, but not brainstem or cortical whisker patterns, after infraorbital nerve injury at birth

1993 ◽  
Vol 336 (2) ◽  
pp. 243-260 ◽  
Author(s):  
Theodore A. Henderson ◽  
Robert W. Rhoades ◽  
Carol A. Bennett-Clarke ◽  
Pat A. Osborne ◽  
Eugene M. Johnson ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Trigeminal Ganglion ◽  
Infraorbital Nerve

scholarly journals TLR8 in the Trigeminal Ganglion Contributes to the Maintenance of Trigeminal Neuropathic Pain in Mice

2020 ◽  
Author(s):  
Lin-Xia Zhao ◽  
Ming Jiang ◽  
Xue-Qiang Bai ◽  
De-Li Cao ◽  
Xiao-Bo Wu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Inflammatory Cytokines ◽  
Trigeminal Ganglion ◽  
Dorsal Root ◽  
Mechanical Allodynia ◽  
Infraorbital Nerve ◽  
Trigeminal Neuropathic Pain ◽  
Intracellular Ca ◽  
Significant Health ◽  
Pro Inflammatory Cytokines

AbstractTrigeminal neuropathic pain (TNP) is a significant health problem but the involved mechanism has not been completely elucidated. Toll-like receptors (TLRs) have recently been demonstrated to be expressed in the dorsal root ganglion and involved in chronic pain. Here, we show that TLR8 was persistently increased in the trigeminal ganglion (TG) neurons in model of TNP induced by partial infraorbital nerve ligation (pIONL). In addition, deletion or knockdown of Tlr8 in the TG attenuated pIONL-induced mechanical allodynia, reduced the activation of ERK and p38-MAPK, and decreased the expression of pro-inflammatory cytokines in the TG. Furthermore, intra-TG injection of the TLR8 agonist VTX-2337 induced pain hypersensitivity. VTX-2337 also increased the intracellular Ca2+ concentration, induced the activation of ERK and p38, and increased the expression of pro-inflammatory cytokines in the TG. These data indicate that TLR8 contributes to the maintenance of TNP through increasing MAPK-mediated neuroinflammation. Targeting TLR8 signaling may be effective for the treatment of TNP.

Chemokine CXCL13 activates p38 MAPK in the trigeminal ganglion after infraorbital nerve injury

Inflammation ◽  
2017 ◽  
Vol 40 (3) ◽  
pp. 762-769 ◽  
Author(s):  
Qian Zhang ◽  
Ming-Di Zhu ◽  
De-Li Cao ◽  
Xue-Qiang Bai ◽  
Yong-Jing Gao ◽  
...  
Keyword(s):  
Nerve Injury ◽  
P38 Mapk ◽  
Trigeminal Ganglion ◽  
Infraorbital Nerve

scholarly journals Increase in IGF-1 Expression in the Injured Infraorbital Nerve and Possible Implications for Orofacial Neuropathic Pain

2019 ◽  
Vol 20 (24) ◽  
pp. 6360 ◽  
Author(s):  
Shiori Sugawara ◽  
Masamichi Shinoda ◽  
Yoshinori Hayashi ◽  
Hiroto Saito ◽  
Sayaka Asano ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Mechanical Allodynia ◽  
Transient Receptor Potential ◽  
Cervical Spinal Cord ◽  
Receptor Potential ◽  
Infraorbital Nerve ◽  
Transient Receptor Potential Vanilloid ◽  
Whisker Pad

Insulin-like growth factor-1 (IGF-1) is upregulated in the injured peripheral nerve bundle and controls nociceptive neuronal excitability associated with peripheral nerve injury. Here, we examined the involvement of IGF-1 signaling in orofacial neuropathic pain following infraorbital nerve injury (IONI) in rats. IONI promoted macrophage accumulation in the injured ION, as well as in the ipsilateral trigeminal ganglion (TG), and induced mechanical allodynia of the whisker pad skin together with the enhancement of neuronal activities in the subnucleus caudalis of the spinal trigeminal nucleus and in the upper cervical spinal cord. The levels of IGF-1 released by infiltrating macrophages into the injured ION and the TG were significantly increased. The IONI-induced the number of transient receptor potential vanilloid (TRPV) subfamily type 4 (TRPV4) upregulation in TRPV subfamily type 2 (TRPV2)-positive small-sized, and medium-sized TG neurons were inhibited by peripheral TRPV2 antagonism. Furthermore, the IONI-induced mechanical allodynia was suppressed by TRPV4 antagonism in the whisker pad skin. These results suggest that IGF-1 released by macrophages accumulating in the injured ION binds to TRPV2, which increases TRPV4 expression in TG neurons innervating the whisker pad skin, ultimately resulting in mechanical allodynia of the whisker pad skin.

Expression of pannexin-1 in the trigeminal ganglion after chronic constriction injury of the infraorbital nerve in a rat model

Neuroreport ◽  
2017 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Yue Zhang ◽  
Dawei Zhu ◽  
Jilei Wang ◽  
Liangxin Yang ◽  
Liecheng Wang ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Rat Model ◽  
Chronic Constriction Injury ◽  
Infraorbital Nerve ◽  
Pannexin 1

scholarly journals Oxytocin-Dependent Regulation of TRPs Expression in Trigeminal Ganglion Neurons Attenuates Orofacial Neuropathic Pain following Infraorbital Nerve Injury in Rats

2020 ◽  
Vol 21 (23) ◽  
pp. 9173
Author(s):  
Masatoshi Ando ◽  
Yoshinori Hayashi ◽  
Suzuro Hitomi ◽  
Ikuko Shibuta ◽  
Akihiko Furukawa ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Infraorbital Nerve ◽  
Transient Receptor Potential Vanilloid ◽  
Withdrawal Threshold ◽  
Whisker Pad ◽  
Ganglion Neurons

We evaluated the mechanisms underlying the oxytocin (OXT)-induced analgesic effect on orofacial neuropathic pain following infraorbital nerve injury (IONI). IONI was established through tight ligation of one-third of the infraorbital nerve thickness. Subsequently, the head withdrawal threshold for mechanical stimulation (MHWT) of the whisker pad skin was measured using a von Frey filament. Trigeminal ganglion (TG) neurons innervating the whisker pad skin were identified using a retrograde labeling technique. OXT receptor-immunoreactive (IR), transient receptor potential vanilloid 1 (TRPV1)-IR, and TRPV4-IR TG neurons innervating the whisker pad skin were examined on post-IONI day 5. The MHWT remarkably decreased from post-IONI day 1 onward. OXT application to the nerve-injured site attenuated the decrease in MHWT from day 5 onward. TRPV1 or TRPV4 antagonism significantly suppressed the decrement of MHWT following IONI. OXT receptors were expressed in the uninjured and Fluoro-Gold (FG)-labeled TG neurons. Furthermore, there was an increase in the number of FG-labeled TRPV1-IR and TRPV4-IR TG neurons, which was inhibited by administering OXT. This inhibition was suppressed by co-administration with an OXT receptor antagonist. These findings suggest that OXT application inhibits the increase in TRPV1-IR and TRPV4-IR TG neurons innervating the whisker pad skin, which attenuates post-IONI orofacial mechanical allodynia.

scholarly journals Tissue-resident M2 macrophages directly contact primary sensory neurons in the sensory ganglia after nerve injury

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Haruki Iwai ◽  
Koji Ataka ◽  
Hajime Suzuki ◽  
Ashis Dhar ◽  
Eriko Kuramoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Nerve Injury ◽  
Bone Marrow Cell ◽  
Trigeminal Ganglion ◽  
Peripheral Nerve Injury ◽  
Marrow Cell ◽  
Infraorbital Nerve ◽  
Sensory Ganglia ◽  
Wild Type ◽  
Satellite Glial Cells

Abstract Background Macrophages in the peripheral nervous system are key players in the repair of nerve tissue and the development of neuropathic pain due to peripheral nerve injury. However, there is a lack of information on the origin and morphological features of macrophages in sensory ganglia after peripheral nerve injury, unlike those in the brain and spinal cord. We analyzed the origin and morphological features of sensory ganglionic macrophages after nerve ligation or transection using wild-type mice and mice with bone-marrow cell transplants. Methods After protecting the head of C57BL/6J mice with lead caps, they were irradiated and transplanted with bone-marrow-derived cells from GFP transgenic mice. The infraorbital nerve of a branch of the trigeminal nerve of wild-type mice was ligated or the infraorbital nerve of GFP-positive bone-marrow-cell-transplanted mice was transected. After immunostaining the trigeminal ganglion, the structures of the ganglionic macrophages, neurons, and satellite glial cells were analyzed using two-dimensional or three-dimensional images. Results The number of damaged neurons in the trigeminal ganglion increased from day 1 after infraorbital nerve ligation. Ganglionic macrophages proliferated from days 3 to 5. Furthermore, the numbers of macrophages increased from days 3 to 15. Bone-marrow-derived macrophages increased on day 7 after the infraorbital nerve was transected in the trigeminal ganglion of GFP-positive bone-marrow-cell-transplanted mice but most of the ganglionic macrophages were composed of tissue-resident cells. On day 7 after infraorbital nerve ligation, ganglionic macrophages increased in volume, extended their processes between the neurons and satellite glial cells, and contacted these neurons. Most of the ganglionic macrophages showed an M2 phenotype when contact was observed, and little neuronal cell death occurred. Conclusion Most of the macrophages that appear after a nerve injury are tissue-resident, and these make direct contact with damaged neurons that act in a tissue-protective manner in the M2 phenotype. These results imply that tissue-resident macrophages signal to neurons directly through physical contact.

scholarly journals Trigeminal Nerve Injury ErbB3/ErbB2 Promotes Mechanical Hypersensitivity

2012 ◽  
Vol 117 (2) ◽  
pp. 381-388 ◽  
Author(s):  
Fei Ma ◽  
Liping Zhang ◽  
Karin N. Westlund
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Mechanical Allodynia ◽  
Infraorbital Nerve ◽  
Wild Type ◽  
Transgenic Rats ◽  
Neuregulin 1 ◽  
Mechanical Hypersensitivity ◽  
Trigeminal Neuropathic Pain ◽  
Whisker Pad

Background Chronic constriction injury of the trigeminal infraorbital nerve results in transient analgesia followed by whisker pad mechanical allodynia in rats. Neuregulin 1 expressed on axonal membranes binds receptor tyrosine kinase ErbB, promoting Schwann cell development and remyelination. This study investigated whether orofacial mechanical allodynia is signaled by ErbB3-ErbB2 heterodimers in injured nerves. Methods Whisker pad mechanical allodynia (von Frey stimuli) was quantified in wild type rats and in transgenic rats with Sleeping Beauty transposon mutation for neuregulin 1 transgene. Pain-related behavior was retested after intraperitoneal injection of the ErbB2 inhibitor Lapatinib, an agent shown by others to reduce breast cancer pain. Infraorbital nerve injury was evaluated histologically with myelin and neuronal biomarkers. ErbB3 changes over time were measured with western blots. Results Whisker pad mechanical hypersensitivity began in week 2 in wild type rats (3.11 ± 5.93 g vs. 18.72 ± 0.00 g after sham surgery, n = 9, P < 0.001), indicating trigeminal neuropathic pain, but was not evident in transgenic rats (odds ratio: 1.12, 95% confidence interval: 0.38-3.35). Initiation of statistically significant mechanohypersensitivity was delayed until week 6 after surgery in transgenic rats (3.44 ± 4.60 g vs. 18.72 ± 0.00 g, n = 4, P < 0.001). Mechanical allodynia, which persisted 8 weeks in wild type rats was alleviated by Lapatinib (15 ± 3.89 g vs. 2.45 ± 1.13 g, n = 6, P < 0.001). Infraorbital nerve damage was verified histologically. Statistically significant ErbB3 increases (weeks 5 and 10) in wild type and transgenic rats (week 10) coincided with time points when mechanical hypersensitivity was present. Conclusion The Neuregulin 1-ErbB3-ErbB2 complex is a causal mechanism in nerve injury-induced trigeminal neuropathic pain. Understanding peripheral glial mechanisms after nerve injury will improve neuropathic pain treatment.

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