Abstract
It has been reported that TMJ inflammation causes an increase in background activity and evoked responses in C- and/or Aδ-primary afferent fibers innervated in inflamed tissues, resulting in peripheral sensitization. Long lasting hyperexcitability of the primary afferent fibers and trigeminal ganglion neurons modulate excitability of trigeminal spinal nucleus neurons, causing central sensitization. These peripheral and central changes in neuronal excitability are thought to be involved in an abnormal TMJ pain.
In order to clarify the peripheral and central mechanisms of TMJ pain, many researchers studied the neuronal activity and induction of neuropeptides in the peripheral and/or central nervous system using the rat model with TMJ inflammation. We analyzed a single neuronal activity and phosphorylated extracellular signal-regulated kinase (PERK) -LI cells in the trigeminal spinal nucleus caudalis (Vc) of rats with CFA-induced TMJ inflammation. The background activity and evoked responses of Vc neurons were increased 3 days after CFA injection into TMJ capsule, the receptive fields of these neurons expanded. These data suggest that central sensitization is induced in Vc neurons 3 days after TMJ inflammation, resulting in the acute TMJ pain.
TMJ chronic inflammation also caused strong pERK expression in dorsal portion of Vc neurons during passive jaw movement. The pERK-LI cells were increased following increase in frequency and intensity of jaw movement. These findings suggest that the dorsal portion of the rostral Vc is involved in mediating chronic pain following TMJ inflammation and that the intracellular ERK cascade is involved.
