The nociceptive jaw-opening reflex: evidence for alpha 2 adrenoceptor involvement

The ability of alpha adrenoceptor agonists to modulate the tooth pulp stimulation evoked (TPS) jaw-opening reflex (JOR) was investigated in rats and rabbits. Low doses of clonidine (6.25-50 micrograms/kg, IV) significantly increased dEMG thresholds. These effects were antagonized by alpha 2 adrenoceptor antagonists (e.g., yohimbine), but not by alpha 1 adrenoceptor antagonists (e.g., prazosin) or mu receptor antagonists (e.g., naloxone). Polar alpha 2 adrenoceptor agonists (e.g., ST-91 and 4-hydroxyclonidine) that cross the blood brain barrier (BBB) poorly and lipophilic alpha 1 adrenoceptor agonists (e.g., ST-587) that cross the BBB easily were without affect on the TPS-JOR. Structures of the peripheral efferent neurocircuitry of the JOR (e.g., the digastric muscle and the neuromuscular junction of the digastric muscle and its motor nerve, the mylohyoid) were shown not to be active sites of clonidine's effect on the TPS-JOR. Treatment with phentolamine (an alpha adrenoceptor antagonist that poorly crosses the BBB) completely poorly crosses the BBB) completely antagonized clonidine's initial transient cardiovascular (pressor) effect without altering its TPS-JOR effects. Pretreatment with reserpine (a catecholamine depleting agent) failed to alter clonidine's affects on the TPS-JOR. Our studies suggest that alpha 2 adrenoceptors potently modulate the TPS-JOR and such modulation may be important in understanding trigeminal neuronal circuitries that partake in pain processing.