Iontophoretic analysis of the pharmacologic mechanisms responsible for initiation and modulation of trigeminal motoneuronal discharge evoked by intra-oral afferent stimulation.
This study investigated the effects of iontophoretic application of excitatory amino acid (EAA) and norepinephrine (NE) agonists and antagonists on synaptic transmission to individual jaw-opener motoneurons (digastric) during activation of the jaw-opening reflex (JOR) evoked by stimulation of either fibers within the oral mucosa (OM), or tooth-pulp (TP). During both OM and TP stimulation, kynurenic acid (KYN), a wide-spectrum EAA antagonist, suppressed jaw-opener motoneuron discharge. Application of APV, an NMDA receptor antagonist, also suppressed motoneuron discharge evoked by TP stimulation, but produced minimal effects on motoneuron discharge evoked by OM stimulation. These data suggest a role of EAA in mediating synaptic transmission from last-order interneurons to jaw-opener motoneurons during the jaw-opening reflex evoked by intra-oral stimulation. Iontophoretic application of NE produced dual effects (facilitation or suppression) on motoneuronal discharge evoked by OM or TP stimulation. The effects were not related to the mode of motoneuronal activation. Iontophoretic application of the alpha 1 agonist, phenylephrine, facilitated motoneuronal discharge. In contrast, application of the alpha 2 agonist, clonidine, suppressed motoneuronal discharge during intra-oral stimulation. These effects were antagonized by prior iontophoretic application of the alpha 1 antagonist, prazosin, or the alpha 2 antagonist, yohimbine, respectively. In those cells in which the predominant effect of NE application on synaptic transmission was either facilitation or suppression of motoneuronal discharge, prior iontophoretic application of prazosin or yohimbine, respectively, antagonized the effects of NE application. These data suggest that NE can modulate synaptic transmission to jaw-opener motoneurons evoked by intra-oral stimulation via activation of alpha 1 or alpha 2 adrenoreceptors on trigeminal motoneurons.
Department of Kinesiology, University of California, Los Angeles 90024.
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Katakura
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Chandler
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D003000:Clonidine / Q000494:pharmacology; D003782:Dental Pulp / Q000294:innervation*; D005071:Evoked Potentials / Q000187:drug effects; D006168:Guinea Pigs; D007736:Kynurenic Acid / Q000494:pharmacology; D008297:Male; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D009061:Mouth Mucosa / Q000294:innervation*; D009334:Neck Muscles / Q000294:innervation / Q000502:physiology; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects; D014059:Tongue / Q000294:innervation*; D014276:Trigeminal Nerve / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
D010656:Phenylephrine; D015016:Yohimbine; D015763:2-Amino-5-phosphonovalerate; D007736:Kynurenic Acid; D003000:Clonidine; D009638:Norepinephrine; D011224:Prazosin