Neurochemical effects of photobiostimulation in the trigeminal ganglion after inferior alveolar nerve injury.
Orofacial pain is associated with peripheral and central sensitization of trigeminal nociceptive neurons. Nerve injury results in release of chemical mediators that contribute to persistent pain conditions. The activation of the transient receptor potential vanilloid 1 (TRPV1), promotes release of calcitonin gene-related peptide (CGRP) and substance P (SP) from trigeminal nerve terminals. CGRP and SP contribute to the development of peripheral hyperalgesia. The expression of SP and CGRP by primary afferent neurons is rapidly increased in response to peripheral inflammation. CGRP receptor activation promotes activation of AMPA receptors, leading to increased firing of neurons which is reflected as central sensitization. In this study we investigated whether inferior alveolar nerve (IAN) injury influences AMPA receptors, CGRP, SP and TRPV1 expression in the trigeminal ganglion (TG). The relative expression of the protein of interest from naive rats was compared to those from injured rats and animals that received low level laser therapy (LLLT). IAN-injury did not change expression of GluA1, GluA2 and CGRP, but increased the expression of TRPV1 and SP. LLLT increases GluA1 and GluA2 expression and decreases TVPV1, SP and CGRP. These results, together with previous behavioral data, suggest that IAN-injury induced changes in the proteins analyzed, which could impact on nociceptive threshold. These data may help to understand the molecular mechanisms of pain sensitization in the TG.
Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paula, SP, Brazil.
D O
DO
Martins
Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paula, SP, Brazil.|University Nove de Julho, São Paulo, SP, Brazil
F M
FM
Santos
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
L R G
LR
Britto
School of Dentistry, University of São Paulo, São Paulo, SP, Brazil.
J B D
JB
Lemos
Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paula, SP, Brazil.
M
M
Chacur
D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000235:genetics / Q000378:metabolism; D020220:Facial Nerve Injuries / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000532:radiotherapy*; D005786:Gene Expression Regulation / Q000528:radiation effects*; D028022:Low-Level Light Therapy; D008297:Male; D008340:Mandibular Nerve / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D009475:Neurons, Afferent / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D010775:Photic Stimulation / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013373:Substance P / Q000235:genetics / Q000378:metabolism; D050916:TRPV Cation Channels / Q000235:genetics / Q000378:metabolism; D012668:Trigeminal Ganglion / Q000293:injuries / Q000378:metabolism / Q000528:radiation effects*
D015740:Calcitonin Gene-Related Peptide; D018091:Receptors, AMPA; D013373:Substance P; D050916:TRPV Cation Channels; C493922:Trpv1 protein, rat; C104722:glutamate receptor ionotropic, AMPA 2