Pannexin 1 role in the trigeminal ganglion in infraorbital nerve injury-induced mechanical allodynia.
Oral Dis
; 29(4): 1770-1781, 2023 May.
Article
em En
| MEDLINE
| ID: mdl-35029007
ABSTRACT
OBJECTIVES:
The detailed pathological mechanism of orofacial neuropathic pain remains unknown. We aimed to examine the pannexin 1 (Panx1) signaling in the trigeminal ganglion (TG) involvement in infraorbital nerve injury (IONI)-induced orofacial neuropathic pain. MATERIALS ANDMETHODS:
Mechanical head-withdrawal threshold (MHWT) was measured in IONI-treated rats receiving intra-TG Panx1 inhibitor or metabotropic glutamate receptor 5 (mGluR5) antagonist administration and MHWTs in naive rats receiving intra-TG mGluR5 agonist administration post-IONI. Glutamate and Panx1 in the TG were measured post-IONI. Panx1, mGluR5, and glutamine synthetase expression in TG were immunohistochemically identified, and changes in the number of mGluR5-P2X3 -expressed TG neurons were examined.RESULTS:
MHWT was significantly decreased post-IONI, and this decrease was reversed by Panx1 inhibition or mGluR5 antagonism. mGluR5 agonism induced a decrease in the MHWT. IONI increased extracellular glutamate in TG. Panx1 was expressed in satellite glial cells and TG neurons, and intra-TG mGluR5 antagonism decreased the number of mGluR5 and P2X3 positive TG neurons post-IONI.CONCLUSIONS:
IONI facilitates glutamate release via Panx1 that activates mGluR5 which was expressed in the nociceptive TG neurons innervating the orofacial region. In turn, P2X3 receptor-expressed TG neurons are enhanced via mGluR5 signaling, resulting in orofacial neuropathic pain.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Hiperalgesia
/
Neuralgia
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article