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Abstract
The trigeminal ganglion (TG) refers to sensory neurons bodies that innervate the spinal cord and peripheral axons that innervate teeth. The tetrodotoxin-sensitive sodium (NA) channels (Nav1.7) play important roles in the pathophysiology of pain. In this study, we investigated the TG expression of Nav1.7 and extracellular signal-regulated kinase (ERK) in a rat model of pulpitis to explore the correlation between these channels and inflammatory pain. Pulpitis was confirmed by hematoxylin-eosin staining. In this study, we demonstrated that the reflex of rats to mechanical stimulation increases after pulp exposure and that the exposed rat molar pulp can upregulate the expression of Nav1.7 and ERK in the rat TG. Three days after rat pulp exposure, the expression levels of the two ion channels in the TG increased. TG target injection of PF04856264, a Nav1.7 inhibitor, dose-dependently increased the mechanical pain threshold and was able to inhibit ERK expression. TG target injection of PD98059, an ERK inhibitor, dose-dependently increased the mechanical pain threshold. These factors simultaneously resulted in the highest production. In this study, with the established link to inflammatory pain, we found that Nav1.7 and ERK both play important roles in the induction of inflammatory pain caused by pulpitis. We also found a correlation between the expression levels of Nav1.7 and ERK and the degree of inflammatory pain. Furthermore, ERK signaling pathways were promoted by the Nav1.7 in TG after pulpitis.
Highlights
The main cause of dental pain is due to pulpitis
There was a correlation between the expression levels of Nav1.7 and degree of inflammatory pain
There was a correlation between the expression levels of Nav1.7 and extracellular signal-regulated kinase (ERK) and the degree of inflammatory pain [48]
Summary
The TG consists of sensory neuronal bodies, the central and peripheral axons of which innervate the spine and teeth, respectively [1]. Changes in primary afferent neurons result in increased excitability [2, 3], which induces the generation of hyperalgesia [4]. These functional changes must be regulated by specific signaling systems in neurons [5]. Voltage-gated sodium channels (VGSCs) govern the electrical excitability of peripheral nerves and play an important role in the pathophysiology of pain. Nav1.7 is an important element of VGSC expression in peripheral nerves. Nav1.7 in nociceptors plays a central role in skeletal muscle nociceptive sensitization [8]
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