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 ◽  
...  
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 ◽  
...  

2020 ◽  
Vol 21 (23) ◽  
pp. 9173
Author(s):  
Masatoshi Ando ◽  
Yoshinori Hayashi ◽  
Suzuro Hitomi ◽  
Ikuko Shibuta ◽  
Akihiko Furukawa ◽  
...  

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.


Oral Diseases ◽  
2022 ◽  
Author(s):  
Ryoko Kurisu ◽  
Tadashi Saigusa ◽  
Yuri Aono ◽  
Yoshinori Hayashi ◽  
Suzuro Hitomi ◽  
...  

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Haruki Iwai ◽  
Koji Ataka ◽  
Hajime Suzuki ◽  
Ashis Dhar ◽  
Eriko Kuramoto ◽  
...  

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.


2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Dulguun Batbold ◽  
Masamichi Shinoda ◽  
Kuniya Honda ◽  
Akihiko Furukawa ◽  
Momoko Koizumi ◽  
...  

Life Sciences ◽  
2019 ◽  
Vol 227 ◽  
pp. 122-128 ◽  
Author(s):  
L.T. Melo ◽  
V. Panchalingam ◽  
P. Cherkas ◽  
A.R. Campos ◽  
L. Avivi-Arber ◽  
...  

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