The present study investigated inflammatory hypersensitivity following compression of the trigeminal ganglion in rats. Experiments were carried out on male Sprague-Dawley rats weighing 250-260 g. Under anesthesia, rats were mounted on a stereotaxic frame and injected with 8μL of 4% agar solution through a stainless steel injector to compress the trigeminal ganglion. In the control group, rats underwent a sham operation without agar injection. Injection sites were examined with a light micrograph after compression of the trigeminal ganglion. Air-puff thresholds (mechanical allodynia) were evaluated 3 days before surgery and 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Air-puff thresholds significantly decreased after compression of the trigeminal ganglion. Mechanical allodynia was established within 3 days and remained strong over 24 days, returning to preoperative levels approximately 40 days following compression. After subcutaneous injection of 5% formalin (50μL) in the compression of the trigeminal ganglion-treated rats, nociceptive scratching behavior was recorded for 9 successive 5-min internals. Injection of formalin into the vibrissa pad significantly increased the number of scratches and duration of noxious behavioral responses in sham-treated rats. Noxious behavioral responses induced by subcutaneous formalin administration were significantly potentiated in rats with trigeminal ganglion compression. These findings suggest that compression of the trigeminal ganglion enhanced formalin-induced infla-mmatory pain in the orofacial area.

It has been well known that excitatory amino acids, primarily glutamate, are involved in the transmission of nociception in pathological and physiological conditions in the spinal and brainstem level. Recently, peripheral glutamate also play a critical role in the peripheral nociceptive transmissions. The present study investigated the role of N-methyl-D-aspartic acid (NMDA) or non-NMDA ionotropic glutamate receptors in formalin-induced TMJ pain. Experiments were carried out on male Sprague-Dawley rats weighing 220-280 g. Intra-articular injection was performed under halothane anesthesia. Under anesthesia, AP-7 (10, 100μM, 1mM/20 μL), a NMDA receptor antagonist, or CNQX disodium salt (0.5, 5, 50, 500 μM/20 μL), a non-NMDA receptor antagonist, were administered intra-articularly 10 min prior to the application of 5% formalin. For each animal, the number of behavioral responses, such as rubbing and/or scratching the TMJ region, was recorded for nine successive 5-min intervals. Intra-articular pretreatment with 1 mM of AP-7 or 50 μM CNQX significantly decreased the formalin-induced scratching behavioral responses during the second phase. Intra-articular pretreatment with 500μM of CNQX significantly decreased the formalin-induced scratching behavior during both the first and the second phase. These results indicate that the intra-articular administration of NMDA or non-NMDA receptor antagonists inhibit formalin-induced TMJ nociception, and peripheral ionotropic glutamate receptors may play an important role in the TMJ nociception.

The response of hepatic mixed function oxygenase (MFO) system was investigated in olive flounder exposed to formalin. Hepatic microsome of olive flounder incubated in vitro with formalin demonstrated the induction of cytochrome P450 (CYP), ethoxyresorufin