The location of the central rhythm generator involved in the cortically induced rhythmical masticatory jaw-opening movement was studied in the ketamine-anesthetized guinea pig. These studies show that a population of neurons is activated by a nonrhythmical input from the cortical masticatory area (CMA) and produces a rhythmical output to the trigeminal motoneurons innervating the jaw-opening muscles. Repetitive stimulation (30 Hz) of the pyramidal tract (PT) rostral to the middle level of the medulla oblongata, in the animal with a precollicular transection as well as with an intact neuraxis, induced a rhythmical reciprocal EMG activity in the anterior digastric and masseter muscles. The rhythmical activity could be monitored by a rhythmical burst in the efferent discharge in the mylohyoid nerve innervating the anterior digastric muscle. Essentially the same pattern was observed when stimulating the PT as that induced by repetitive stimulation of the CMA. The rhythmical efferent burst in the mylohyoid nerve could still be induced after paralyzing the animal. Repetitive PT stimulation in the isolated brain stem after precollicular and bulbospinal transections induced a rhythmical pattern in the anterior digastric EMG and an efferent activity in the mylohyoid nerve. The rhythmical mylohyoid nerve burst could be induced after paralyzing the animal. After section of the medial part of the brain stem at the pontobulbar junction, including the PT, repetitive PT stimulation at the pontine level did not induce any masticatory activity either in the digastric EMG or in the efferent discharge in the mylohyoid nerve, while stimulation at the rostral bulbar level still induced a rhythmicity that was essentially the same pattern as before the section. By testing the effects of total and partial transections of the brain stem in coronal and sagittal planes at various locations, we found that the medial bulbar reticular formation, the lateral pons including the trigeminal motor nucleus and nerve, and the reticulotrigeminal motoneuronal pathways composed the minimum structures that must be left intact to induce a rhythmicity in the anterior digastric EMG and the efferent discharge in the mylohyoid nerve by repetitively stimulating the PT. Repetitive PT stimulation induced a field potential in the medial bulbar reticular formation, which periodically fluctuated in the masticatory rhythm coincident with the rhythmical activity in the digastric EMG. This fluctuation persisted in the same rhythm after paralysis of the animal.(ABSTRACT TRUNCATED AT 400 WORDS)

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1. Single-unit activity was recorded from neurons in the bulbar parvocellular reticular formation (PCRF) dorsal and dorsolateral to the gigantocellular reticular nucleus near its caudal boundary, and the roles of these reticular neurons in induction of rhythmical activity of trigeminal motoneurons by repetitive stimulation of the cerebral cortex (the cortical masticatory area, CMA) were studied in the paralyzed guinea pig anesthetized with urethan or with ketamine and chlorpromazine. 2. One hundred nine PCRF neurons were activated antidromically by microstimulation in either the masseter (MA) or anterior digastric (AD) motoneuron pool in the ipsilateral trigeminal motor nucleus, and orthodromically by stimulation in the contralateral CMA. Repetitive CMA stimulation induced rhythmical burst activity in these PCRF neurons in association with the rhythmical field potential in the contralateral AD motoneuron pool induced by the same CMA stimulation. The burst was synchronous with the rhythmical AD field potential in 81 neurons, 44 and 37 of which responded antidromically to stimulation in the MA and AD motoneuron pools, respectively. The remaining 28 neurons antidromically responded to stimulation in the MA motoneuron pool, and their burst corresponded in time with the period between successive AD field potentials. 3. Spike-triggered averaging of the intracellular potentials of MA and AD motoneurons (MNs) by simultaneously recorded spontaneous spikes of the PCRF neurons, which showed rhythmical burst responses during the jaw-opening phase to repetitive CMA stimulation, revealed a monosynaptic inhibitory postsynaptic potential in MA.MNs in 12 of 34 tested pairs and a monosynaptic excitatory postsynaptic potential (EPSP) in AD.MNs in 14 of 26 tested pairs. An EPSP was also found in MA.MNs after a monosynaptic latency from triggering spikes in 11 of 37 tested PCRF neurons that showed burst activity during the jaw-closing phase. 4. We conclude that both excitatory and inhibitory premotor neurons projecting to MA.MNs as well as excitatory premotor neurons projecting to AD.MNs are located in the PCRF, and that these premotor neurons relay the output of the central rhythm generator for rhythmical jaw movements in the medial bulbar reticular formation to trigeminal motoneurons, and thus participate in induction of rhythmical activities of trigeminal motoneurons by repetitive CMA stimulation.

The role of the pyramidal tract (PT) in the induction of the rhythmical masticatory activity (RMA) of the anterior digastric motoneurons by repetitive stimulation of the cortical masticatory area (CMA) was studied in the ketamine-anesthetized guinea pig. The coronal section of the medial brain stem at the pontine level did not show any effect on the cortically induced RMA in the digastric EMG, as long as the majority of the PT fibers was spared of the section. In contrast, unilateral section of the PT at the pontine level abolished the RMA in the digastric EMG induced by repetitive stimulation of the ipsilateral CMA, while that induced by the contralateral CMA stimulation was not affected by the PT section. The threshold of repetitive PT stimulation for induction of the RMA of the digastric EMG was much higher at the levels caudal to the facial nucleus than that at more rostral levels, and no RMA was induced by the PT stimulation at the caudal bulbar levels even at the supramaximal intensities for RMA induction of the PT stimulation at more rostral levels. Single shocks applied to the PT at the caudal bulbar levels did not evoke any antidromic field potential in the CMA. Single shocks applied to the CMA evoked a negative field potential in the medial bulbar reticular formation (MBRF) mainly on the contralateral side after a monosynaptic latency, which was largest in amplitude in the region including the most dorsal portion of the nucleus reticularis paragigantocellularis and the area dorsally adjacent to it (dPGC). Stimulation of the oral portion of the nucleus reticularis gigantocellularis (GC) evoked an antidromic negative field potential in the ipsilateral dPGC. Intracellular recording from neurons in the dPGC demonstrated that neurons were located in the dPGC that responded with EPSPs after a monosynaptic latency to single shocks applied to the contralateral CMA and with antidromic spike potentials to stimulation of the oral portion of the ipsilateral GC (GCo). Single shocks applied to the dPGC evoked antidromic field potential in the area in the contralateral cerebral cortex corresponding with the CMA. Injection of horseradish peroxidase (HRP) into the dPGC on one side retrogradely labeled the pyramidal cells with HRP bilaterally in the cerebral cortical area corresponding with the CMA. The number and density of the labeled cells on the contralateral side far exceeded those on the ipsilateral side.(ABSTRACT TRUNCATED AT 400 WORDS)

Neurons found in the medial bulbar reticular formation were activated by stimulation of the orbital gyrus and responded with antidromic spike potentials to selective stimulation of either the masseter or anterior digastric motoneuron pool in the trigeminal motor nucleus in cats anesthetized with alpha-chloralose. These two kinds of reticular neurons were assumed to be inhibitory neurons projecting to masseter motoneurons (IM neurons) and excitatory neurons projecting to anterior digastric motoneurons (ED neurons), involved in the effects of stimulation of the orbital gyrus on trigeminal motoneurons: inhibition of masseter motoneurons and excitation of anterior digastric motoneurons. Input-output properties of IM and ED neurons were studied intracellularly with the following results: (1) stimulation of the orbital gyrus evoked EPSPs in IM and ED neurons with mono- and polysynaptic latencies; and (2) stimulation of the lingual nerve evoked a spike potential in a few IM and ED neurons after a rather long latency, indicating that the pathways involved in the cortical control of trigeminal motoneurons via IM and ED neurons were basically separate from those responsible for the reflex control by the peripheral inputs. Intracellular injection of horseradish peroxidase revealed that both IM and ED neurons were small or medium in size and the former were smaller than the latter, while none of the large reticular neurons directly projected to the trigeminal motor nucleus. This suggests a possible functional differentiation among bulbar reticular neurons according to cell size.