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The electromyograph (EMG) activity of the left anterior digastric and the genioglossus muscles was studied in ketamine-anesthetized guinea pigs under 3 separate jaw movement paradigms. The first paradigm has been previously named spontaneous rhythmic jaw movements. These jaw movements occur 1–2 h after the onset of ketamine anesthesia. After spontaneous rhythmic jaw movements began, a single dose of apomorphine caused a new, second jaw movement paradigm to occur, apomorphine-induced rhythmic jaw movements. The final paradigm, cortically-evoked rhythmic jaw movements, was elicited by electrical stimulation of the masticatory area of the cerebral cortex. Genioglossus EMG activity was complex and highly variable in spontaneous rhythmic jaw movements; however, apomorphine-induced jaw movements were characterized by simultaneously occurring rhythmic EMG bursts of approximately 230 ms duration in both the digastric and genioglossus muscles. In 4 of 5 animals, genioglossus muscle activity onset preceded digastric muscle activity onset by approximately 20 ms. These results support the hypothesis that apomorphine-induced rhythmic jaw movements are an analog of lapping in the awake animal. In cortically-evoked rhythmic jaw movements, both digastric and genioglossus EMG activity were time-locked to the cortical electrical stimulation, with an onset latency of approximately 11 ms for the digastric EMG activity and of 16 ms for the genioglossus EMG activity. These results support the hypothesis that both trigeminal and hypoglossal motoneuron pools are closely coupled in certain coordinative movement patterns.

Herpes simplex virus (HSV) infection induces numerous electrophysiological and microscopic changes in neurons in vitro. To investigate the effect of HSV infection on in vivo neuronal activity, we induced an acute, latent and reactivated HSV infection of the trigeminal ganglia of guinea pigs through orofacial HSV inoculation and studied its effect on the trigeminal jaw-opening reflex of anesthetized guinea pigs. During the acute viral infection period both the threshold for elicitation of the reflex, and the latency to the onset of the reflex response were increased. During the latent viral infection in the trigeminal ganglia, the jaw-opening reflexes in the viral infected animals were not different from those of non-infected control animals. However, reactivation of the latent viral infection in these animals resulted in increases in both the threshold and latency of the jaw-opening reflex. These changes were similar to those found in animals with the acute viral infection. These results indicate that acute or reactivated latent HSV infection of the nervous system results in functional changes in the reflex pathways involving the trigeminal gasserian ganglia and brainstem neurons harboring infectious HSV-1.

In the ketamine/urethane anesthetized guinea pig, electromyographic (EMG) responses of the anterior digastric muscle were studied when loci within the lower brainstem were microejected with lidocaine (2%) during rhythmical jaw movements (RJMs) evoked by repetitive electrical stimulation of the masticatory area of the cortex. The area investigated was between the trigeminal motor nucleus (Mot V) and the rostral pole of the inferior olive. Microejections of lidocaine, contralateral to the cortical stimulus site, into the ventral-medial portion of Mot V where digastric motoneurons are known to be located, resulted in reduction or complete abolishment of the digastric EMG activity ipsilateral to the ejection with no effective change in mean cycle duration (CD) or mean percent normalized integrated amplitude of the contralateral digastric EMG. Microejections of lidocaine, contralateral to the cortical stimulus site, into the ponto-medullary reticular formation in areas that included portions of the caudal nucleus pontis caudalis (PnC), nucleus gigantocellularis (GC), medial nucleus parvocellularis (PCRt), and dorsal paragigantocellularis (dPGC), in most cases produced abilateral reduction in the mean normalized integrated amplitude and a bilateral increase in the mean cycle duration. In these sites, the bilateral increase in mean cycle duration of digastric EMG bursts was also associated with a significant increase of coefficient of variation in CD. In many cases, microejection of lidocaine completely abolished rhythmical digastric activity, bilaterally. HRP injections into Mot V were performed to determine the locations of trigeminal premotoneurons and their relationship to effective lidocaine sites for rhythmical jaw movement suppression. Retrogradely labeled cells were found mainly in the mesencephalic nucleus of V; trigeminal principal and spinal V sensory nuclei, bilaterally; and within the intermediate and lateral regions of reticular formation,bilaterally. No labeling was found in the medial reticular formation, including the nucleus gigantocellularis and dorsal paragigantocellularis. The results of this study indicate that regions in the lower brainstem, including portions of the nuclei gigantocellularis and dorsal paragigantocellularis, may participate in masticatory timing and pattern formation, lending further support to the previous hypothesis that (1) both GC and dPGC nuclei of the medial reticular formation contain components of the oscillatory network necessary for RJM production; (2) this regiondoes not contain trigeminal premotoneurons, suggesting a segregation between central timing neurons within these regions of brainstem and trigeminal premotoneurons; and (3) ipsilateral cortex activates neurons located contralaterally within the brainstem reticular core which are critical forbilateral digastric EMG activity during cortically induced RJMs.

The excitability of lingual and inferior dental nerve terminals in the trigeminal main sensory nucleus was increased following a conditioning stimulus delivered to the same nerves of the contralateral side. The lingual nerve primary afferent depolarization (PAD) began at a shorter CS-TS interval (CS, conditioning stimulus; TS, test stimulus), and reached a maximum level of depolarization sooner, than did the PAD evoked in the inferior dental nerve. This difference in the time course of the PAD was not dependent on the site of the CS; i.e. , the same time course was observed for the lingual nerve terminals whether the CS was delivered to either the contralateral lingual, or inferior dental nerve. The effect of the contralateral CS was also tested on the ipsilateral lingual-digastric and inferior dental-digastric reflexes in order to determine if the PAD observed in the ipsilateral nerve terminals would be reflected in similar changes in reflexes mediated by those nerves. It was found that both digastric reflexes were inhibited by the CS. The time course of the inhibition showed similar characteristics to that of the previously discussed PAD; i.e., the onset of the lingual-digastric reflex inhibition began a shorter CS-TS interval and reached maximum effectiveness sooner than did the inhibition of the inferior dental-digastric reflex. The possible significance of the results in relation to the role of presynaptic inhibitory mechanisms in the reflex control of jaw movement is discussed.

We have investigated the effects of systemic administration of a glycine antagonist, strychnine, on rhythmical jaw movements (RJMs) induced by repetitive stimulation of the masticatory area of the guinea pig cerebral cortex. It was found that after strychnine administration (0.4 mg/kg), the frequency of the cortically induced RJMs was minimally affected, whereas the burst durations of the digastric EMG during the jaw opening phase of the RJM cycle were dramatically increased. These data suggest that the neuronal network (central pattern generator (CPG)) which is responsible for the production of rhythmical jaw movements is not critically dependent upon glycine for the genesis of the basic oscillatory rhythm. On the other hand, glycine synapses are involved with the neuronal mechanisms which are responsible for controlling the burst durations of the digastric muscle during the jaw opening phase of each rhythmic jaw movement cycle.

Intracellular recordings were carried out in extensor hindlimb motoneurons during l -DOPA-induced fictive locomotion from acute and chronically spinalized cats. It was demonstrated that motoneurons in chronic animals exhibited irregularly occuring, high frequency discharges within a given burst of a spike train, and sporadic membrane potential depolarizations and hyperpolarizations correlated with extensor and flexor nerve filament activity, respectively, during the locomotor cycle. In contrast, motoneurons recorded from acute cats demonstrated smooth membrane potential fluctuation and regularly occuring low frequency spike discharges. These results indicate that the pharmacologically activated central pattern generator (CPG) for locomotion in young adult chronic cats spinalized at two weeks of age produces disorganized locomotor-like patterns in the absence of sensory feedback. It is suggested that the above-mentioned characteristics of membrane potential fluctuations and spike discharges are not due to alterations in the motoneuron membrane properties, but instead are due to changes in the inputs to the motoneurons.

Summary During periods of increased presynaptic excitability, antidromic motoneuron activation triggers a centrifugal dorsal root discharge in the cat spinal cord. The present study was concerned with the type of motoneuron and dorsal root fibers involved in this motoneuron-presynaptic interaction as well as with its mechanism. The experiments were carried out in acute spinal cats. By conduction velocity studies it was shown that only alpha motoneurons and primary afferent fibers belonging to group I muscle afferents participate in the interaction. The central time of the motoneuron-presynaptic interaction was approximately 0.4 msec and was always at least 0.2 msec shorter than the monosynaptic reflex. The hypothesis is put forward that via an antidromic electrical interaction, the motoneuron discharge can depolarize the same presynaptic terminals which, through chemical synaptic mechanisms, induce the orthodromic firing of the same neuron.

The central pattern generator (CPG) for rhythmical jaw movements (RJMs) was activated, in the anesthetized guinea pig, by systemic injection of a specific dopamine agonist, apomorphine (APO). It was shown that APO induced RJMs required an intact superior colliculus, and were blocked by low doses (0.05-1.0 mg/kg) of haloperidol (HAL), a dopamine antagonist. This is in contrast to the neural pathways mediating RJMs evoked by repetitive electrical stimulation of the masticatory cortex which remained effective following both lesions of the superior colliculus and administration of HAL. These results suggest that there are at least two anatomically separate and pharmacologically distinct command centers for activation of the CPG for RJMs in the guinea pig.

The effects of systemic injections of a serotonin agonist (quipazine), and antagonist (methysergide), on rhythmical jaw movements (RJMs) in the ketamine anesthetized guinea pig were examined. It was observed that quipazine, (1) significantly elevated the electrical threshold for inducing RJMs by repetitive stimulation of the masticatory cortex and (2) reduced the amplitude of the digastric and masseter EMG activity during RJMs. In contrast, the excitability of the short latency pathway from masticatory cortex to digastric motoneurons, and the excitability of the digastric reflex evoked by electrical stimulation of the mucosa of the tongue were not significantly affected by quipazine administration. Methysergide administration had little effect on the threshold for evoking RJMs, and on the excitability of the digastric reflex and short latency pathway from cortex to digastric motoneurons. These data suggest that the central pattern generator (CPG) for RJMs is not critically dependent upon serotonin receptor activation since RJMs can be induced after methysergide administration. On the other hand, excitation of the CPG by repetitive cortical stimulation can be inhibited by serotonin receptor activation. These results are interpreted as supporting our previously described model of RJM production by repetitive cortical stimulation.

Vertical and horizontal jaw movements along with lateral pterygoid (PT) and anterior digastric (DIG) muscle electromyogram (EMG) activity were recorded in anesthetized guinea pigs during electrical stimulation of the masticatory area of cortex. Both repetitive stimulation at 25 Hz and short pulse-train stimulation (3 pulse, 500 Hz) delivered 2/s produced jaw opening with a horizontal component contralateral to the side of cortex stimulated in addition to short latency (7–12 ms) evoked EMG bursts in the ipsilateral PT muscle and in the DIG muscles bilaterally. Evidence was also obtained which indicated that both types of cortical stimulation resulted in time-locked inhibition of the contralateral PT muscle. Unlike each short train of stimulus pulses, however, each pulse in the repetitive train did not evoke jaw movement and EMG bursts of a consistent amplitude. Rather, repetitive stimulation produced rhythmical movements of the jaw associated with recurrent periods of activity and inactivity in the EMG records. These results demonstrate the presence of a corticotrigeminal pathway between masticatory cortex and PT motoneurons in addition to a similar pathway to DIG motoneurons, and suggest that both pathways are similarly modulated by a central pattern generator to produce rhythmical jaw movements.

The EMG activity of the left anterior digastric muscle as well as associated jaw movements were studied in ketamine-anesthetized guinea pigs that had received i.v. infusions of angiotensin II (ANG-II). Rhythmic jaw movements with two distinct movement profiles were associated with ANG-II infusion. One movement profile was typified by vertical jaw opening and closing movements with little or no associated horizontal movement. The second rhythmical jaw movement profile was unlike the first in that jaw closing was accompanied by a significant horizontal deflection of the jaw. Both jaw movement profiles were similar in that little or no horizontal movement occurred during jaw opening. Tongue protrusions were also observed during jaw opening in both cases. The results show that ANG-II induces rhythmic jaw movements in anesthetized guinea pigs. ANG-II-induced jaw movement profiles and digastric muscle EMG activity are similar to those seen after an i.v. injection of apomorphine in the anesthetized guinea pig, and to those associated with lapping in the awake animal.

Physiological evidence is presented for the presence of stretch reflexes in the lateral pterygoid (Pt) muscle of the guinea pig. The central reflex effects of excitation of Pt stretch reflex afferents were also investigated. Passive lateral jaw displacement, which resulted in stretch of the Pt muscle on the side of jaw movement and stretch of the zygomatico-mandibularis (Z) muscle on the side contralateral to the movement, evoked increased EMG activity in these muscles. Stimulation of the trigeminal mesencephalic nucleus (mes V) evoked monosynaptic reflexes in both the Pt and Z nerves. Tonic stretch of the Pt muscle facilitated the monosynaptic reflex in the Pt nerve evoked by stimulation of mes V. Tonic vibration of the Pt muscle facilitated the mes V evoked monosynaptic reflex in the nerves to the ipsilateral Pt and contralateral Z muscles. Conversely, tonic vibration of the Z muscle facilitated the monosynaptic reflex evolved by mes V stimulation in the contralateral Pt and ipsilateral Z nerve. The results support the view that muscle spindles exist in the Pt and Z muscles and that there is a monosynaptic stretch reflex for both the Pt and Z muscles with cell bodies located in the mes V nucleus. It was also shown that the ipsilateral Pt muscle and the contralateral Z muscle act as synergists in the production of lateral jaw movements and that the organization of the stretch reflexes originating from the Pt and Z muscles support their synergistic action.

Summary o 1. Effects of stimulation of the central cut end of the hypoglossal nerve on the masseteric reflex were studied in cats (spinal cord sectioned between C 2 and C 3 ). Hypoglossal stimulation with 1–3 pulses induced a prolonged suppression of the ipsilateral and contralateral masseteric reflex, with or without a facilitatory phase following the peak of suppression. 2. The threshold of suppression was 2–3 times higher than the threshold for firing axons of hypoglossal motor neurons and maximal suppression was obtained when the hypoglossal nerve was stimulated with pulses supramaximal for these axons. Pulses of longer duration than necessary to induce suppression were usually required to induce facilitation. 3. Hypoglossal influences on the masseteric reflex were almost completely abolished following section of the hypoglossal roots on the stimulated side, whereas the effects still remained following section of the glossopharyngeal, vagal and accessory nerve roots and the dorsal roots of C 1 and C 2 when the hypoglossal roots were left intact. 4. Dihydro-β-erythroidine did not alter the hypoglossal effects on the masseteric reflex. 5. Neither precollicular nor medullo-spinal transection altered these hypoglossal influences, whereas ponto-medullary transection completely abolished them. 6. From these results it was concluded that afferent impulses in the hypoglossal nerve enter the brain stem primarily through the hypoglossal roots, ascend bilaterally in the brain stem via a polysynaptic route to the trigeminal motor nucleus and induce inhibition and facilitation of the masseteric monosynaptic reflex.

The nature of the suppression of the masseteric monosynaptic reflex due to stimulation of the orbital gyrus was investigated by intracellular recording from massetteric motoneurons. The following results were obtained: (1) Either single pulses or pulse trains delivered to the orbital gyrus usually exerted a prolonged suppression (up to around 40 msec) of the masseteric monosynaptic reflex recorded along the masseteric nerve in response to stimulation of the trigeminal mesencephalic nucleus or the masseteric nerve itself. (2) The antidromic focal potential, recorded within the trigeminal motor nucleus in response to the stimulation of the masseteric nerve, was remarkably suppressed by stimulation of the orbital gyrus. (3) For intracellular studies, masseteric motoneurons were identified by anti-dromic spike potentials induced by stimulation of the masseteric nerve. Monosynaptic EPSPs were recorded in these masseteric motoneurons in response to stimulation of the trigeminal mesencephalic nucleus, confirming the monosynaptic excitatory linkage between the mesencephalic and the motor nucleus of the trigeminal nerve. (4) Stimulation of the orbital gyrus induced a prolonged hyperpolarizing potentials in masseteric motoneurons, the time course of which closely resembled that of the cortically induced suppression of the masseteric monosynaptic reflex. Monosynaptic, as well as antidromic, spikes of masseteric motoneurons were inhibited coincident with this hyperpolarizing potential. Hyperpolarization was changed to depolarization by the intracellular diffusion of Cl−. (5) Simultaneous recording of monosynaptic spikes in masseteric motoneurons and the masseteric reflex evoked by stimulation of the mesencephalic nucleus of V revealed a close temporal correlation between inhibition of the monosynaptic spikes and suppression of masseteric monosynaptic reflex. (6) It was concluded that an active postsyna[tic inhibition is primarily responsible for the observed suppression of the massteric monosynaptic reflex by electrical stimulation of the orbital gyrus.