• Pain · Feb 1981

    Raphe-induced suppression of the jaw-opening reflex and single neurons in trigeminal subnucleus oralis, and influence of naloxone and subnucleus caudalis.

    • Barry J Sessle and James W Hu.
    • Division of Biological Sciences, Faculty of Dentistry, University of Toronto, Toronto, Ont. M5G 1G6 Canada.
    • Pain. 1981 Feb 1; 10 (1): 19-36.

    Abstract(1) The effects of stimulation of the nucleus raphe magnus (NRM) and the periaqueductal gray (PAG) were tested on the digastric (jaw-opening) reflex and on the activity of functionally identified single neurons recorded in trigeminal (V) subnucleus oralis in the brain stem. Reflex and neuronal responses evoked by tooth pulp stimulation could be readily suppressed for 250--1000 msec by PAG and NRM conditioning stimuli. The effects were not specific for tooth pulp afferent inputs, however, since suppression was also apparent in jaw-opening reflex responses evoked by low-intensity electrical or tactile stimulation of oral-facial sites, and in the mechanically or electrically evoked responses of oralis neurons with localized low-threshold mechanoreceptive fields. (2) The modulatory effects on the jaw-opening reflex and oralis neuron activity were not altered by reversible cold block of synaptic transmission in V subnucleus caudalis. Thus it appears that the PAG- and NRM-induced effects on the reflex and oralis neurons are not dependent on relays via caudalis. (3) Some of the suppressive influences on responses to oral-facial stimuli could be reversed by the administration of the opiate antagonist naloxone. This suggests that some of the modulatory influences involve endogenous opiate-related mechanisms. (4) Many of the oralis neurons were identified as trigeminothalamic relay neurons on the basis of their antidromic response to ventrobasal thalamic stimulation; PAG and NRM conditioning produced not only a suppression of their orthodromic responses to oral-facial stimuli but also caused a decrease in the antidromic excitability of the relay neurons. This decrease may be indicative of raphe-induced postsynaptic inhibition of oralis neurons, and/or presynaptic facilitation of their thalamic endings.

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