Microinfusions of excitatory amino acid antagonists into the trigeminal sensory complex antagonize the jaw opening reflex in freely moving rats.

Microinfusions of EAA antagonists (APV 0.1 microliter 25 mM, gamma-DGG 0.1 microliter 50 mM, CNQX 0.1 microliter 50 mM, ketamine 0.1 microliter 0.2 M) were performed in freely moving rats while recording the long latency jaw opening reflex (JOR) elicited by electrical stimulation of the dental pulp. NMDA and non-NMDA antagonists were applied in the trigeminal sensory complex at the termination of dental pulp afferents. The selective NMDA antagonist APV strongly reduced the amplitude of the polysynaptic JOR. gamma-DGG and ketamine, which are broader spectrum NMDA antagonists, showed similar effects with some variations in their kinetics. CNQX, an antagonist for non-NMDA receptor subtypes, failed to affect the JOR. The results suggest that long latency JOR requires activation of NMDA receptors, while the early component elicited by periodontal afferents does not. These NMDA-receptors could belong either to JOR interneurons activated by tooth pulp afferents or to digastric motoneurons, receiving the inputs through a polysynaptic pathway. Recent anatomical results favour the first hypothesis while not excluding the second.