Presynaptic excitability changes produced in brain stem endings of tooth pulp afferents by raphe and other central and peripheral influences

Abstract

1. (1) In view of the association of tooth pulp stimulation with pain, and the possibility that nociceptive transmission may be presynaptically modulated by endogenous opiate-related mechanisms, we examined the presynaptic modulatory effects of peripheral and central conditioning stimuli on the excitability of brain stem endings of tooth pulp primary afferents in anesthetized or decerebrate cats. A presynaptic excitability effect was measured as a change in the amplitude of the antidromic compound action potential recorded from the pulp or as a change in the probability of antidromic activation of single pulp primary afferents recorded either in the trigeminal (V) ganglion or directly from the pulp. 2. (2) A total of 195 single tooth pulp afferents supplying the ipsilateral maxillary or mandibular canine teeth was recorded. The majority conducted in the A-delta range, although about 25 % had conduction velocities indicative of faster conducting axons. The excitability of the brain stem endings of the pulp afferents could be increased by conditioning stimuli delivered to the periaqueductal gray (PAG) and nucleus raphe magnus (NRM), as well as by noxious and non-noxious stimuli applied to oral-facial and more remote sites, and by stimulation of the cerebral cortex. 3. (3) The presynaptic effects induced in pulp endings in V subnucleus oralis by raphe stimulation do not rely on the integrity of V subnucleus caudalis which is considered the important brain stem relay site for oral-facial pain. This was shown by the inability of reversible cold block of synaptic transmission in caudalis to alter presynaptic excitability increases induced in oralis. Nonetheless, the cold block procedure did reveal that caudalis exerts a tonic presynaptic ascending facilitatory influence on the pulp afferent input to oralis neurons. 4. (4) Since tooth pulp afferents are predominantly, if not exclusively, related to pain, it is noteworthy that our studies with the opiate antagonist naloxone failed to provide any substantive evidence that the presynaptic modulatory effects on pulp afferent endings are opiate-related. Only in one of 25 pulp afferents tested did naloxone reduce the PAD effect induced by PAG, NRM or afferent conditioning. These findings do not support the view that the descending raphe influences operate through a presynaptic opiate-related mechanism on nociceptive transmission, at least as far as the tooth pulp afferent input to the brain stem is concerned.