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Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury

Trigeminal nerve injury causes a distinct time window of glial activation in the trigeminal spinal subnucleus caudalis (Vc), which are involved in the initiation and maintenance phases of orofacial neuropathic pain. Microglia-derived factors enable the activation of astrocytes. The complement compon...

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Autores principales: Asano, Sayaka, Hayashi, Yoshinori, Iwata, Koichi, Okada-Ogawa, Akiko, Hitomi, Suzuro, Shibuta, Ikuko, Imamura, Yoshiki, Shinoda, Masamichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7560139/
https://www.ncbi.nlm.nih.gov/pubmed/32957694
http://dx.doi.org/10.3390/ijms21186834
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author Asano, Sayaka
Hayashi, Yoshinori
Iwata, Koichi
Okada-Ogawa, Akiko
Hitomi, Suzuro
Shibuta, Ikuko
Imamura, Yoshiki
Shinoda, Masamichi
author_facet Asano, Sayaka
Hayashi, Yoshinori
Iwata, Koichi
Okada-Ogawa, Akiko
Hitomi, Suzuro
Shibuta, Ikuko
Imamura, Yoshiki
Shinoda, Masamichi
author_sort Asano, Sayaka
collection PubMed
description Trigeminal nerve injury causes a distinct time window of glial activation in the trigeminal spinal subnucleus caudalis (Vc), which are involved in the initiation and maintenance phases of orofacial neuropathic pain. Microglia-derived factors enable the activation of astrocytes. The complement component C1q, which promotes the activation of astrocytes, is known to be synthesized in microglia. However, it is unclear whether microglia–astrocyte communication via C1q is involved in orofacial neuropathic pain. Here, we analyzed microglia-astrocyte communication in a rat model with infraorbital nerve injury (IONI). The orofacial mechanical hypersensitivity induced by IONI was significantly attenuated by preemptive treatment with minocycline. Immunohistochemical analyses revealed that minocycline inhibited the increase in c-Fos immune-reactive (IR) cells and the fluorescence intensity of both Iba1 and glial fibrillary acidic protein (GFAP) in the Vc following IONI. Intracisternal administration of C1q caused orofacial mechanical hypersensitivity and an increase in the number of c-Fos-IR cells and fluorescence intensity of GFAP. C1q-induced orofacial mechanical hypersensitivity was completely abrogated by intracisternal administration of fluorocitrate. The present findings suggest that the enhancement in the excitability of Vc nociceptive neurons is produced by astrocytic activation via the signaling of C1q released from activated microglia in the Vc following IONI, resulting in persistent orofacial neuropathic pain.
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spelling pubmed-75601392020-10-22 Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury Asano, Sayaka Hayashi, Yoshinori Iwata, Koichi Okada-Ogawa, Akiko Hitomi, Suzuro Shibuta, Ikuko Imamura, Yoshiki Shinoda, Masamichi Int J Mol Sci Article Trigeminal nerve injury causes a distinct time window of glial activation in the trigeminal spinal subnucleus caudalis (Vc), which are involved in the initiation and maintenance phases of orofacial neuropathic pain. Microglia-derived factors enable the activation of astrocytes. The complement component C1q, which promotes the activation of astrocytes, is known to be synthesized in microglia. However, it is unclear whether microglia–astrocyte communication via C1q is involved in orofacial neuropathic pain. Here, we analyzed microglia-astrocyte communication in a rat model with infraorbital nerve injury (IONI). The orofacial mechanical hypersensitivity induced by IONI was significantly attenuated by preemptive treatment with minocycline. Immunohistochemical analyses revealed that minocycline inhibited the increase in c-Fos immune-reactive (IR) cells and the fluorescence intensity of both Iba1 and glial fibrillary acidic protein (GFAP) in the Vc following IONI. Intracisternal administration of C1q caused orofacial mechanical hypersensitivity and an increase in the number of c-Fos-IR cells and fluorescence intensity of GFAP. C1q-induced orofacial mechanical hypersensitivity was completely abrogated by intracisternal administration of fluorocitrate. The present findings suggest that the enhancement in the excitability of Vc nociceptive neurons is produced by astrocytic activation via the signaling of C1q released from activated microglia in the Vc following IONI, resulting in persistent orofacial neuropathic pain. MDPI 2020-09-17 /pmc/articles/PMC7560139/ /pubmed/32957694 http://dx.doi.org/10.3390/ijms21186834 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Asano, Sayaka
Hayashi, Yoshinori
Iwata, Koichi
Okada-Ogawa, Akiko
Hitomi, Suzuro
Shibuta, Ikuko
Imamura, Yoshiki
Shinoda, Masamichi
Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury
title Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury
title_full Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury
title_fullStr Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury
title_full_unstemmed Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury
title_short Microglia–Astrocyte Communication via C1q Contributes to Orofacial Neuropathic Pain Associated with Infraorbital Nerve Injury
title_sort microglia–astrocyte communication via c1q contributes to orofacial neuropathic pain associated with infraorbital nerve injury
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7560139/
https://www.ncbi.nlm.nih.gov/pubmed/32957694
http://dx.doi.org/10.3390/ijms21186834
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