Photobiomodulation and B vitamins administration produces antinociception in an orofacial pain model through the modulation of glial cells and cytokines expression.

Chronic constriction injury (CCI) of infraorbital nerve (IoN) results in whisker pad mechanical allodynia in rats and activation glial cells contributing to the development of orofacial pain. Whisker pad mechanical allodynia (von Frey stimuli) was tested pre and postoperatively and conducted during the treatment time. Photobiomodulation (PBM) and vitamins B complex (VBC) has been demonstrated therapeutic efficacy in ameliorate neuropathic pain. The aim of this study was to evaluate the antinociceptive effect of PBM, VBC or the combined treatment VBC â€‹+ â€‹PBM on orofacial pain due to CCI-IoN. Behavioral and molecular approaches were used to analyses nociception, cellular and neurochemical alterations. CCI-IoN caused mechanical allodynia and cellular alterations including increased expression of glial fibrillary acid protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba-1), administration of VBC (B1/B6/B12 at 180/180/1.8 â€‹mg/kg, s.c., 5 times all long 10 sessions) and PBM therapy (904 â€‹nm, power of 75Wpico, average power of 0.0434 â€‹W, pulse frequency of 9500 â€‹Hz, area of the beam 0.13 â€‹cm2, 18 â€‹s duration, energy density 6 â€‹J/cm2, with an energy per point of 0.78 â€‹J for 10 sessions) or their combination presented improvement of the nociceptive behavior and decreased expression of GFAP and Iba-1. Additionally, CCI-IoN rats exhibited an upregulation of IL1ß, IL6 and TNF-α expression and all treatments prevented this upregulation and also increased IL10 expression. Overall, the present results highlight the pain reliever effect of VBC or PBM alone or in combination, through the modulation of glial cells and cytokines expression in the spinal trigeminal nucleus of rats.

Early and late behavioral changes in sciatic nerve injury may be modulated by nerve growth factor and substance P in rats: a chronic constriction injury long-term evaluation.

Chronic constriction injury (CCI) simulates the symptoms of chronic nerve compression, which is characterized by allodynia and hyperalgesia. Nerve growth factor (NGF) is released after nerve injury by immune and Schwann cells and transported in retrograde fashion to the dorsal root ganglion (DRG), resulting in increased synthesis of Substance P (SP) and the triggering of neuropathic pain. Here we performed long-term evaluation of allodynia and hyperalgesia in a CCI model, and evaluated the effects of NGF and SP on the peripheral and central nervous systems. Most previous studies have shown deficits and molecular changes 14 days after surgery, however, the long-term effects have not been evaluated. We performed Randall-Selitto, Von Frey, Hargreaves and acetone tests for the entire 56 days post-surgery. Several of these deficits increased 14 to 56 days after CCI and we measured a constant increase in NGF levels in the DRG and spinal cord over the course of the experiment. In contrast, SP optical density maintained enhanced expression in DRG tissue from 14 to 56 days after CCI, whereas it was significantly increased only 56 days post-surgery in spinal cord. We perform long-term evaluation of symptoms associated with CCI and measure associated molecular changes. Moreover, by characterizing the behavioral signatures of this model, our work supports future studies.