OBJECTIVE: To test the hypothesis that peripheral N-methyl-D-aspartate (NMDA) receptors play a role in pain induced by experimental tooth movement. MATERIALS AND METHODS: Male Sprague-Dawley rats weighing between 200 g and 300 g were used in this study. Expression of NMDA receptors subunit 1 (NMDAR1) in the mandibular portion of the trigeminal ganglion (TG) was determined by Western blotting 4 hours and 1, 2, 3, 5, 7, and 14 days after tooth movement. Changes in the time taken by the rats on nocifensive behavior then effects of NMDA receptor antagonist MK-801 and force magnitude on these changes in behavior and NMDAR1 expression were evaluated. RESULTS: Experimental tooth movement led to a statistically significant increase in NMDAR1 expression at protein level from day 1 to 7 after force application initiating tooth movement. Time spent on nocifensive behavior dramatically increased from day 1 to 7. The rhythm in NMDAR1 expression in the TG and behavioral activities correlated well with the initial orthodontic pain responses. The magnitude of the nocifensive behavior and NMDAR1 expression were both force magnitude dependent and could be reduced by peripheral NMDA receptor antagonist MK-801. CONCLUSIONS: The hypothesis is accepted. Peripheral NMDA receptors are modulated by experimental tooth movement and involved in the development of tooth movement pain.
OBJECTIVE: To test the hypothesis that peripheral N-methyl-D-aspartate (NMDA) receptors play a role in pain induced by experimental tooth movement. MATERIALS AND METHODS: Male Sprague-Dawley rats weighing between 200 g and 300 g were used in this study. Expression of NMDA receptors subunit 1 (NMDAR1) in the mandibular portion of the trigeminal ganglion (TG) was determined by Western blotting 4 hours and 1, 2, 3, 5, 7, and 14 days after tooth movement. Changes in the time taken by the rats on nocifensive behavior then effects of NMDA receptor antagonist MK-801 and force magnitude on these changes in behavior and NMDAR1 expression were evaluated. RESULTS: Experimental tooth movement led to a statistically significant increase in NMDAR1 expression at protein level from day 1 to 7 after force application initiating tooth movement. Time spent on nocifensive behavior dramatically increased from day 1 to 7. The rhythm in NMDAR1 expression in the TG and behavioral activities correlated well with the initial orthodontic pain responses. The magnitude of the nocifensive behavior and NMDAR1 expression were both force magnitude dependent and could be reduced by peripheral NMDA receptor antagonist MK-801. CONCLUSIONS: The hypothesis is accepted. Peripheral NMDA receptors are modulated by experimental tooth movement and involved in the development of tooth movement pain.