Jaw-opening Motoneurons Research Articles

Trigeminal motoneuron responses to vestibular stimulation in the guinea pig.

Experiments performed in the guinea pig were aimed at evaluating the effect of electric or caloric stimulations of the vestibular afferents on the electrical activity of the jaw-closing and jaw-opening trigeminal motoneurons. Results showed that masseter and digastric motoneurons mainly responded to vestibular ampullar activation with excitatory responses, with latencies being shorter for contralateral than ipsilateral ampullar stimulation. Differences in latencies between the jaw-closing and jaw-opening trigeminal motoneurons were observed: the masseter motoneurons constantly responded about 2 msec earlier than the digastric motoneurons. These results suggest that the vestibular-trigeminal relationship is quite complex and uses multiple systems to connect the vestibular apparatus with the trigeminal motor nuclei. From the functional point of view, the vestibular-trigeminal relationship may play a role in the dynamic control of the jaw muscle tone during head movements.

Musculotopic organization in the motor trigeminal nucleus of the reeler mutant mouse

We examined the musculotopic organization in the motor trigeminal nucleus and the somatotopical arrangement in the trigeminal ganglion of the normal and reeler mice. To determine whether or not masticatory motoneurons are malpositioned in the reeler mouse, we injected horseradish peroxidase (HRP) into the masticatory muscles of normal and reeler mice. Injections of HRP into the jaw-closing muscles, i.e., the masseter and temporalis muscles, labeled large multipolar neurons in the dorsolateral division of the motor trigeminal nucleus of both normal and reeler mice. Similar injections into the jaw-opening muscles, i.e., the anterior belly of the digastric muscle and mylohyoid muscle, labeled large multipolar neurons in the ventromedial division of the motor trigeminal nucleus of both mouse strains. Thus, the normal myotopical arrangement of the masticatory muscles on the motor trigeminal nucleus is preserved in the reeler mouse. However, detailed analysis revealed that jaw-opening motoneurons were more widely scattered in the reeler mouse than in the normal control. To examine the somatotopical arrangement of the first-order sensory neurons in the trigeminal ganglion of the normal and reeler mice, we subcutaneously injected Fast blue (FB) into the mental region and Diamidino yellow (DY) into the vibrissal region of the same animals. No differences in distribution patterns of FB-labeled and DY-labeled neurons in the whole-mounted trigeminal ganglion could been seen between these two strains, suggesting that migration of trigeminal ganglion cells, which are derived from the neural crest and placode, is not deranged by the reeler genetic locus.

The control of jaw-opener motoneurons during active sleep

Brainstem and spinal cord motoneurons that innervate somatic musculature serving antigravity functions are postsynaptically inhibited during active sleep [3,12,22,23]. However, it has been reported that hypoglossal motoneurons (which do not innervate antigravity muscles) are not postsynaptically inhibited during active sleep, but are disfacilitated [16,17]. In the present report we describe changes, during active sleep, in the excitability and membrane potential of digastric and synergistic motoneurons of the trigeminal motor pool; these neurons do not perform antigravity functions [21]. The experiments described in the present report were performed in chronic cats that were prepared for intracellular recording. The motoneurons hyperpolarized an average of 11 mV (S.D.± 1.29, n = 8, P < 0.005) during active sleep compared to quiet sleep. Hyperpolarization was accompanied by a reduction in the excitability of the somadendritic regions of the neurons, as indicated by an increase in the delay of propagation of antidromic spikes from the initial segment to the somadendritic portion of the cell. High gain membrane potential recordings from these motoneurons revealed the occurrence of a remarkably large number of hyperpolarizing potentials during active sleep. When K-chloride-filled microelectrodes were utilized and chloride ions were injected intracellularly, the polarity of these potentials was reversed. During phasic episodes of active sleep, there was a clear increase in hyperpolarizing potential activity, a blockade of somadendritic spikes and phasic reductions in the amplitude of the initial segment spikes. Hyperpolarizing potentials occurred in conjunction with ponto-geniculo-occipital waves. These potentials were reversed in polarity when chloride ions were injected into the cells, indicating that motoneurons of the trigeminal motor pool that do not perform antigravity functions are postsynaptically inhibited during active sleep. The similarities between the inhibitory phenomena in these neurons and those observed in jaw-closer and spinal cord motoneurons lead us to conclude that the excitability of trigeminal motoneurons that innervate muscles with reciprocal functions is suppressed by a postsynaptic inhibitory process during active sleep, as are most other somatic motoneurons [3,12,22,23].

Differences in acetylcholinesterase activity between jaw-opening and jaw-closing motoneurons in the rat

Differences in acetylcholinesterase activity between jaw-opening and jaw-closing motoneurons in the rat

Synaptic potentials produced in jaw-closer and jaw-opener motoneurons by palatal stimulation.

Excitation and inhibition of temporal and digastric motoneurons (Temp. and Dig. Mns) during transient jaw closing, the so-called jaw-closing reflex, were studied in cats. Application of diffuse pressure stimulation to the posterior palatal surface produced the jaw-closing reflex and it was found that mechanosensory inputs from the posterior palatal mucosa produce depolarizing potentials on the Temp. Mns responsible for jaw closure during the jaw-closing reflex. We have demonstrated that in one-third of 27 explored Temp. Mns the initial bursts of spikes were elicited before the onset of jaw closure, suggesting that these cells contribute to initiate jaw closure during the jaw-closing reflex. The remaining cells probably contributed to maintain the occlusal phase. Furthermore, it was found that mechanosensory inputs from the posterior palatal mucosa produce a hyperpolarization-depolarization sequence in the Dig. Mns responsible for the jaw-closing reflex. In addition, when pressure stimulation was applied to the anterior palatal mucosa, sustained jaw opening was elicited and an increase of firing frequency of Dig. Mns occurred 40 ms before the onset of jaw opening and continued for 80 ms.

Control of trigeminal motoneurons from the cerebellar interpositus nucleus of the guinea pig.

1. Effects of stimulation of the cerebellar interpositus nucleus (IPN) on jaw reflexes and trigeminal motoneurons were studied along with the route responsible for the effects in ketamine-anesthetized guinea pigs. 2. Stimulation in the IPN evoked a bilateral, ipsilaterally dominant, short-latency reciprocal effect on jaw reflexes: a depression of the jaw-closing masseteric reflex and a facilitation of the jaw-opening digastric reflex. This reciprocal phase was followed by a non-reciprocal facilitatory phase. 3. Stimulation in the IPN evoked a short-latency, strychnine-sensitive inhibitory postsynaptic potential (IPSP) followed by a rebound depolarizing potential in the jaw-closing masseter motoneurons (MAMNs) and an excitatory postsynaptic potential (EPSP) in the jaw-opening anterior digastric motoneurons (ADMNs). The time course of the intracellular response of MAMNs to the IPN stimulation was similar to that of the IPN-induced effects on the jaw-closing reflex. In contrast, the duration of the IPN-induced EPSP in ADMNs was shorter than the IPN-induced facilitation of the jaw-opening reflex. 4. After the IPN neurons were lost by injection of kainic acid into the nucleus, the reciprocal effect of the IPN stimulation on the jaw reflexes could not be seen, even though the projection fibers from the trigeminal sensory nucleus to the IPN remained essentially intact. 5. Stimulation in the superior cerebellar peduncle (SP) induced the same reciprocal effect on the jaw reflexes as the IPN stimulation. A lesion of the SP virtually abolished the reciprocal effect on the jaw reflexes of stimulation in the IPN ipsilateral with reference to the SP lesion. 6. Transection of the brain stem at the level immediately caudal to the red nucleus did not affect the reciprocal effect of the IPN stimulation on the jaw reflexes. 7. We conclude that the IPN output bilaterally induces an inhibition of jaw-closing MAMNs and an excitation of jaw-opening ADMNs, oligosynaptically by way of a direct cerebelloreticular projection system via the SP.

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.

An iontophoretic analysis of the pharmacologic mechanisms responsible for trigeminal motoneuronal discharge during masticatory-like activity in the guinea pig

1. The effects of iontophoretic application of the excitatory amino acid antagonists kynurenic acid (KYN) and DL-2-amino-5-phosphonovaleric acid (APV), as well as the monoamines serotonin (5-HT) and norepinephrine (NE), on extracellularly recorded jaw opener motoneuron [digastric motoneuron (DIG)] discharge during cortically induced rhythmical masticatory-like activity (RMA) were examined in the anesthetized guinea pig. 2. Iontophoretic application of KYN, a broad-spectrum amino acid antagonist, suppressed the motoneuronal discharge evoked by short pulse train stimulation of the cortex for most cells tested. In contrast, iontophoretic application of APV, a specific N-methyl-D-aspartate (NMDA) antagonist, was usually without effect on the motoneuronal discharge evoked by short pulse train stimulation. 3. During RMA evoked by repetitive cortical stimulation, both KYN and APV suppressed rhythmical DIG motoneuronal discharge in many cells tested. 4. These data suggest that excitatory amino acid receptors on jaw opener motoneurons are involved in activation of RMA. It is proposed that the short-latency rapid excitation of jaw opener motoneurons, which occurs during both short pulse train cortical stimulation and RMA induced by repetitive cortical stimulation, is mediated, at least in part, by non-NMDA receptors. It is further suggested that the large-amplitude, long-duration slow rhythmical oscillations, which occur in the membrane potential of jaw opener motoneurons during RMA induced by repetitive cortical stimulation, are mediated, at least in part, by NMDA receptors. 5. Iontophoretic application of NE or 5-HT with low currents (less than 20 nA) produced a facilitation of digastric motoneuronal discharge during cycle-triggered glutamate application, short pulse train cortical stimulation, and RMA evoked by repetitive cortical stimulation. These facilitatory effects on motoneuronal discharge started within 1 min of drug application, reached a peak at approximately 3 min that persisted for several minutes after the application period, and recovered to control levels within 10-15 min. Direct application of NE or 5-HT, in the absence of chemical or synaptic activation, failed to activate these motoneurons. However, iontophoretic application of either monoamine could facilitate and bring to threshold rhythmical motoneuronal discharges during subthreshold repetitive cortical stimulation. 6. Iontophoretic application of methysergide, a 5-HT antagonist, and phentolamine, an alpha adrenoreceptor blocker, both produced a selective and reversible blockade of the facilitatory effects of 5-HT and NE, respectively, on motoneuronal discharge during cortically induced RMA. In contrast, iontophoretic application of sotalol, a beta adrenoreceptor blocker, had no effect on the NE-induced facilitation of RMA.(ABSTRACT TRUNCATED AT 400 WORDS)

Intracellular analysis of trigeminal motoneuron rhythmical activity during stimulation of pontomedullary reticular formation in anesthetized guinea pig.

1. The effects of repetitive stimulation of the nucleus pontis caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation on jaw opener and closer motoneurons were examined. The PnC-Gi was stimulated at 75 Hz at current intensities less than 90 microA. 2. Rhythmically occurring, long-duration, depolarizing membrane potentials in jaw opener motoneurons [excitatory masticatory drive potential (E-MDP)] and long-duration hyperpolarizing membrane potentials [inhibitory masticatory drive potentials (I-MDP)] in jaw closer motoneurons were evoked by 40-Hz repetitive masticatory cortex stimulation. These potentials were completely suppressed by PnC-Gi stimulation. PnC-Gi stimulation also suppressed the short-duration, stimulus-locked depolarizations [excitatory postsynaptic potentials (EPSPs)] in jaw opener motoneurons and short-duration, stimulus-locked hyperpolarizations [inhibitory postsynaptic potentials (IPSPs)] in jaw closer motoneurons, evoked by the same repetitive cortical stimulation. 3. Short pulse train (3 pulses; 500 Hz) stimulation of the masticatory area of the cortex in the absence of rhythmical jaw movements activated the short-latency paucisynaptic corticotrigeminal pathways and evoked short-duration EPSPs and IPSPs in jaw opener and closer motoneurons, respectively. The same PnC-Gi stimulation that completely suppressed rhythmical MDPs, and stimulus-locked PSPs evoked by repetitive stimulation to the masticatory area of the cortex, produced an average reduction in PSP amplitude of 22 and 17% in jaw closer and opener motoneurons, respectively. 4. PnC-Gi stimulation produced minimal effects on the amplitude of the antidromic digastric field potential or on the intracellularly recorded antidromic digastric action potential. Moreover, PnC-Gi stimulation had little effect on jaw opener or jaw closer motoneuron membrane resting potentials in the absence of rhythmical jaw movements (RJMs). PnC-Gi stimulation produced variable effects on conductance pulses elicited in jaw opener and closer motoneurons in the absence of RJMs. 5. These results indicate that the powerful suppression of cortically evoked MDPs in opener and closer motoneurons during PnC-Gi stimulation is most likely not a result of postsynaptic inhibition of trigeminal motoneurons. It is proposed that this suppression is a result of suppression of activity in neurons responsible for masticatory rhythm generation.

Neural mechanism generating firing patterns in jaw motoneurons during the food-induced response in Aplysia kurodai. I. Identification and characterization of premotor neurons.

1. In each right and left buccal ganglia of Aplysia kurodai, we identified 4 premotor neurons impinging on the ipsilateral jaw-closing and -opening motoneurons. Three of them (MA1 neurons) had features of multifunctional neurons. Current-induced spikes in the MA1 neurons produced excitatory junction potentials (EJPs) in the buccal muscle fibers. In addition, tactile stimulation of the buccal muscle surface produced a train of spikes in the MA1 neurons without synaptic input. The other neuron (MA2) had only a premotor function. 2. The MA1 and MA2 neurons had similar synaptic effects on the jaw-closing and -opening motoneurons. Current-induced spikes in the premotor neurons gave rise to monosynaptic inhibitory postsynaptic potentials (IPSPs) in the ipsilateral jaw-closing motoneurons. Simultaneously, spikes in one of the MA1 neurons and the MA2 also gave rise to monosynaptic excitatory postsynaptic potentials (EPSPs) in the ipsilateral jaw-opening motoneuron. 3. The IPSPs and the EPSPs induced by spikes in the premotor neurons were reversibly blocked by d-tubocurarine and hexamethonium, respectively, suggesting that the MA1 and MA2 neurons are cholinergic. 4. When depolarizing and hyperpolarizing current pulses were passed into one premotor neuron, attenuated but similar potential changes were produced in another randomly selected premotor neuron in the same ganglion, suggesting that they are electronically coupled.

Physiological and morphological characteristics of cat masticatory motoneurons—intracellular injection of HRP

The physiology and morphology of masticatory motoneurons of adult cats were examined by the methods of intracellular recording and intracellular injection of horseradish peroxidase. Masseter and jaw-opening motoneurons were identified by intracellular recordings of the antidromic response following stimulation of the masseter and mylohyoid nerves, respectively. An excitatory postsynaptic potential (EPSP) was recorded from masseter neurons by stimulation of the masseter nerve with stimulus intensity below threshold for antidromic response. In contrast, the EPSP was not recorded from jaw-opening motoneurons by stimulation of the mylohyoid nerve with stimulus intensity below threshold for antidromic response. Patterns of postsynaptic potentials (PSPs) in the masseter motoneurons following stimulation of the tooth pulp or periodontal afferents were classified into 4 types: hyperpolarization ( n = 40), depolarization-hyperpolarization ( n = 9), hyperpolarization-depolarization ( n = 5), and depolarization with spike potentials ( n = 10). On the other hand, patterns of the PSPs in the jaw-opening motoneurons following stimulation of the same afferents were classified into two types: depolarization with spike potentials ( n = 19), and hyperpolarization ( n = 5). Twenty-five masseter and 7 jaw-opening motoneurons and an intranuclear neuron were reconstructed from serial sections in the transverse plane. On the basis of dendritic morphology, the masseter motoneurons could be classified into two major groups, type I ( n = 15) and type II ( n = 9), whereas two neurons were found to constitute a separate category of the masseter motoneuron. The dendritic distributions of all the jaw-opening motoneurons examined were generally similar and there was no indication of the existence of subtypes, whereas there were 2 or 3 subgroups in type I and type II masseter motoneurons. Type I masseter neurons had primary dendrites which extended radially in all directions, and the whole profile of their dendritic trees presented a spherical and an egg-shaped appearance. In type II masseter neurons, the origin of primary dendrites was bipolar or tripolar, and the whole profile of their dendritic trees presented a hemispherical and mirror-imaged, funnel-shaped appearance. The other two masseter motoneurons had a particular dendritic tree which was much simpler in configuration, with less tapering or branching than those of other neurons examined. In contrast, the dendritic profiles of all the jaw-opening motoneurons were similarly organized and showed vertically oriented dendritic trees which were more developed in the dorsomedial than in the ventrolateral direction. Dendrites from all groups extended beyond the boundaries of the motor nucleus into the reticular formation. The border between the dorsolateral and ventromedial subdivisions was crossed by some dendrites but the overlap was small. Among neurons examined in the present study, one intranuclear neuron identified had the simplest dendritic tree and smalles soma size, with axon collaterals projecting to the reticular formation. No significant differences in several soma-dendritic parameters were found between morphologically distinct motoneuronal subpopulations and between the jaw-opening and masseter motoneurons. There were no instances in which axon collaterals were observed for the masticatory motoneurons.

Morphology of masticatory motoneurons stained intracellularly with horseradish peroxidase

Masticatory motoneurons were identified electrophysiologically and stained with horseradish peroxidase (HRP). The masseter motoneurons could be divided into 3 groups on the basis of their dendritic morphology. In contrast, the digastric or mylohyoid motoneurons showed a similar dendritic configuration. These neurons had much developed dendritic trees in the dorsomedial than ventrolateral direction. The first group of the masseter motoneurons had their dendritic trees which extended radially in all directions with a slight preference to project rostrally. These somata were located in the center of the subdivision containing the masseter motoneurons. In the second group, their dendritic arbores had a polarity extending hemispherically. These neuronal somata were located in the medial, ventral, and lateral regions of the subdivision. For the masseter motoneurons in the two groups and jaw-opening motoneurons, the dendritic swellings were frequently observed in the distal branches. The third group had their dendritic trees which were much simpler in configurations with less tapering or branching than those of other neurons examined. Furthermore, a wide variety of dendritic spines and appendages, and no dendritic swellings, observed in the third group were distinct from other neurons stained. The dendritic trees of the jaw-closing and -opening motoneurons were confined to the individual subdivisions. There were no instances in which axon collaterals were observed for well-stained 16 axons.

Mode of control of the trigeminal motor neurons by serotonergic input in guinea pigs

Serotonin (5-HT) is known to play an important role in the motor control in various animal species. However, it has not been clarified as yet whether or not these motor effects are induced by the direct effects of 5-HT on the motoneurons. The present study was undertaken to investigate the effect of the iontophoretic application of 5-HT on the activity of the trigeminal (masseter and anterior digastric) motoneurons in the chloralose-anesthetized or decerebrated, paralysed guinea pigs. Multibarrel glass micropipetts were used for the extracellular recording of the single unit activity and the microiontophoretic application of glutamate, 5-HT and methysergide (MSG, a specific antagonist of 5-HT) . The spontaneous as well as the glutamate-induced activity of the majority of masseter motoneurons was enhanced by 5-HT, and it was inhibited by MSG in most of these 5-HT-sensitive masseter motoneurons. The degree of excitation decreased with an increase in the baseline firing rate after the 5-HT application. Similar results were obtained in the anterior digastric rnotoneurons. However, the degree of the excitatory effects of 5-HT was lower than on the masseter motoneurons, and the MSG affected only a few of the anterior digastric motoneurons. The masseteric reflex evoked by the electrical stimulation of the trigeminal mesencephalic nucleus as well as by the stretch of the masseter muscle was enhanced by 5-HT. It was concluded that 5-HT exerts mainly a non-reciprocal facilitatory effect on the jawcloser and jaw-opener motoneurons. Endogenous 5-HT may tonically enhance the excitability of the trigeminal motoneurons.

Control mode of the trigeminal motor neurons from the cerebellar nucleus interpositus

There is a massive projection from the trigeminal sensory complex into the cerebellum, particularly into the nucleus interpositus (IP) . In the present study, the effects of IP stimulation on the trigeminal motoneurons as well as on the jaw reflexes and also the pathways involved in the effects were studied in the ketamine-anesthetized guinea pigs, with the following results: 1) The IP stimulation evoked a short-latency reciprocal effect on the jaw reflexes, bilaterally with an ipsilateral dominance, consisting of the depression of the jaw-closing reflexes and facilitation of the jaw-opening reflexes. 2) The IP stimulation evoked IPSPs in the masseter motoneurons and EPSPs in the anterior digastric motoneurons with essentially the same latency. Their latency and time course were similar to those of the short-latency IP effects on the jaw reflexes. 3) After the lesion of the IP by local injection of kainic acid, the reciprocal IP effect on the jaw reflexes was abolished, although the projection fibers from the trigeminal sensory complex to the IP were left intact. Thus, the IP effects cannot be ascribed to the antidromic stimulation of these cerebellar afferent fibers. 4) Stimulation of the superior cerebellar peduncle (SP) evoked the same effects on the jaw reflexes as the ipsilateral IP stimulation. After the lesion of the SP, the effects of the ipsilateral IP stimulation disappeared. 5) Transection of the brain stem at the level caudal to both the thalamic ventrolateral nucleus and the red nucleus did not affect the effects of IP stimulation on the jaw reflexes. It was concluded that the IP inhibits the jaw-closer motoneurons and excites the jaw-opener motoneurons by way of the SP and possibly via the projection to the lower brain stem reticular formation. This IP effect may contribute to the initiation of mastication, by facilitating the transition of the jaw posture from the closure to the opening position.

そしゃく運動中の延髄網様体ニューロンの活動様式 下あご運動およびそしゃく筋筋電図との相関

Inhibitory premotor neurons projecting to the jaw closer motoneurons (IM neurons) and excitatory premotor neurons projecting to the jaw opener motoneurons (ED neurons) in the bulbar reticular formation were shown to be involved in the inhibition of the jaw closer motoneurons and the excitation of the jaw opener motoneurons during the jaw-opening phase of the cortically induced masticatory rhythm in the immobilized cats. The present study analyzed the role of these bulbar reticular neurons in the control of the natural masticatory jaw movements during food ingestion in the chronically prepared unanesthetized cats. The single unit activity was recorded from 40 bulbar reticular neurons which modulated the firing frequency in the same rhythm as the masticatory jaw movement. Thirty-four neurons showed a burst during the jaw-opening phase (opening type), while the remaining 6 neurons showed a burst during the jaw-closing phase (closing type) . By averaging the full-rectified EMG of the masticatory muscle by the spikes of the reticular neurons, 4 neurons were found to be the IM neurons and the other 4 neurons the ED neurons. All these premotor neurons belonged to the opening type. A posi tive correlation was found between 1) the instantaneous firing frequency (IFF) and the velocity of the jaw movements in 4 of 6 opening type neurons (2 of 3 IM neurons and 2 of 3 ED neurons) and in 3 of the 6 closing type neurons, 2) the IFF and the jaw displacement in 3 of the 6 opening type neurons (2 of 3 IM neurons and 1 of 3 ED neurons) and in 2 of the 6 closing type neurons, 3) the number of spikes in a burst and the duration of the jaw-opening phase or the jawclosing phase as well as the maximum displacement and/or velocity of the jaw movement in 16 tested neurons and 4) the maximum firing frequency and the maximum displacement and/or velocity of jaw movement in the 16 tested neurons. It was concluded that the bulbar reticular neurons were involved in the control of the velocity and displacement of ja movement during mastication by modulating the firing frequency and the number of spikes in a burst.

Axonal trajectories of masticatory motoneurons: A genu formation of axons of jaw-opening motoneurons in the cat

Axonal courses of jaw-opening motoneurons were examined in the cat by applying horseradish peroxidase to the central cut end of the nerve branch which supplies the mylohyoid and/or the anterior digastric muscle. The axons of mylohyoid and anterior digastric motoneurons, which are located in the ventromedial division of the trigeminal motor nucleus, initially swing dorsalward before running ventrolaterally to leave the pons; axons proceeding in the more rostral levels make turns in the more dorsomedial tegmental regions, and those running in the most rostral levels form a small genu in the region near the midline under the floor of the fourth ventricle.

Localization of masticatory motoneurons in the trigeminal motor nucleus of the guinea pig

The myotopical arrangement of masticatory motoneurons was examined in the guinea pig by the horseradish peroxidase method. The trigeminal motor nucleus was composed of dorsolateral and ventromedial divisions; the former was seen in the whole rostrocaudal extent of the nucleus, while the latter was present at levels of the caudal two thirds of the nucleus. The jaw-closer motoneurons were located in the dorsolateral division, and the jaw-opener motoneurons (mylohyoid and anterior digastric motoneurons) were seen in the ventromedial division.

Synaptic basis of orbital cortically induced rhythmical masticatory activity of trigeminal motoneurons in immobilized cats

Synaptic basis of the centrally induced masticatory rhythm was studied by intracellular recording from jaw closer and opener motoneurons during repetitive stimulation of the orbital gyrus (OG) of the encéphale isolé of immobilized cats, with the following results. (1) Repetitive OG stimulation induced a rhythmical alternation of hyperpolarizing and depolarizing potentials in jaw closer motoneurons. Rhythmical efferent burst discharges induced in the digastric nerve by OG stimulation coincided with the hyperpolarizing phase. The hyperpolarizing potential was reversed to a depolarizing potential by intracellular Cl- injection, while the depolarizing potential was not reversed to hyperpolarization, indicating that the hyperpolarizing and depolarizing potentials consisted at least mainly of IPSPs and EPSPs, respectively. (2) Repetitive OG stimulation induced rhythmical depolarizing potentials superimposed by spike bursts in jaw opener motoneurons, corresponding in time with the rhythmical efferent bursts in the digastric nerve. Synaptic activation noise was increased coincidentally with the depolarizing potential, indicating that EPSPs were involved in the generation of the depolarizing potential. No or little hyperpolarization if any was observed between successive depolarizing potentials. (3) Repetitive OG stimulation induced efferent burst discharges in the digastric nerve with the masticatory rhythm unaccompanied by any spike potential in the supratrigeminal neurons responsible for peripherally evoked inhibition of jaw closer motoneurons, indicating that the peripheral inhibitory mechanisms do not play an essential role in the central generation of the masticatory rhythm by OG stimulation.

Intracellular determination of membrane potential of trigeminal motoneurons during sleep and wakefulness.

Intracellular determination of membrane potential of trigeminal motoneurons during sleep and wakefulness.

Postsynaptic potentials in the jaw-opening motoneurons by stimulation of the trigeminal nerves

Postsynaptic potentials in the jaw-opening motoneurons by stimulation of the trigeminal nerves