NEUROPHARMACOLOGICAL MECHANISMS UNDERLYING RHYTHMICAL DISCHARGE IN TRIGEMINAL INTERNEURONS DURING FICTIVE MASTICATION

1. We have examined the effects of iontophoretic application of antago nists to excitatory amino acid (EAA) receptors, as well as gIycine and gamma-aminobutyric acid(GABA), on rhythmically active (RA) brain stem neurons during cortically induced masticatory activity (RMA) in the a nesthetized guinea pig. Ten ofthese neurons were antidromically activa ted at latencies of 0.3-0.9 ms by stimulation of the trigeminal motor nucleus (MoV). 2. RA neurons were divided into closer and opener type according to the phase of activation during RMA. Iontophoretic applica tion of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a specific non-N- methyl-D-aspartate (NMDA) receptor antagonist, suppressed discharge of both closer and opener type RA neurons during RMA. In contrast, ionto phoretic application of -((1)-2-carboxypiperazin-4-yl)-propyl-1-phosph onic acid (CPP), a specific NMDA receptor antagonist, was not effectiv e in suppressing discharge of most opener type RA neurons but did redu ce activity of closer type RA neurons. 3. Spike discharge of most RA n eurons was time locked to each cortical stimulus during RMA. Some of t he RA neurons were activated at a short latency to short pulse train s timulation of the cortex in the absence of RMA. In most cases CNQX red uced such time-locked responses during RMA and greatly reduced dischar ge evoked by short pulse stimulation of the cortex in all cases. In co ntrast, CPP was not as effective in suppressing either the time-locked responses during RMA or the discharge evoked by short pulse train sti mulation of the cortex. 4. D,L-Homocysteic acid (HCA) application prod uced low level maintained discharge in RA neurons before RMA induction . When RMA was evoked in combination with HCA, rhythmical burst discha rges with distinct interburst periods during the opening phase of RMA were observed in most closer type RA neurons. In contrast, during RMA in combination with HCA. application, opener type RA neurons showed bu rst discharges that were modulated during the RMA cycle but lacked dis tinct interburst periods during the closer phase of the cycle. 5. Duri ng application of strychnine (STR), a glycine antagonist, discharge of closer type RA neurons increased in the opener phase of RMA during co ntinuous HCA application. In contrast, bicuculline methiodide (BIC), a GABA antagonist, did not increase unit discharge of closer type RA ne urons in the opener phase of RMA. 6. It is concluded that closer type RA neurons receive, alternatively, EAA-mediated excitatory and glycine -mediated inhibitory masticatory synaptic drive signals during RMA. Fo r closer type RA neurons both non-NMDA and NMDA receptors participate in burst excitation during RMA. In contrast, opener type RA neurons re ceive mainly phasic excitatory masticatory drive signals mediated pred ominately by non-NMDA receptors during burst discharge of RMA with muc h less contribution of phasic inhibition during their interburst perio ds.