No abstract

To elucidate a function of the central amygdaloid nucleus (ACE) in the trigeminal system, the ACE conditioning effect on the jaw-opening reflex (JOR) regarded as a nociceptive reflex was investigated in the cat anesthetized with pentobarbital sodium. The JOR to molar tooth pulp stimulation with an intensity 1.2-1.5 times the threshold was recorded in the ipsilateral digastric muscle. As conditioning stimulation, a train of 33 rectangular pulses (0.5 ms in duration) at 330 Hz with an intensity of 300 microA was applied to the ipsilateral ACE. The conditioning stimulation inhibited a JOR that had a latency of 7.90 +/- 0.88 ms (n = 36). The inhibition was maximum (83.1 +/- 11.2%) at a conditioning-test (C-T) interval of 110 ms and continued for C-T intervals of up to 1,000 ms. Likewise, microinjection of 0.5 M monosodium glutamate (10 microliters) into the ACE-inhibited the JOR for approximately 10 min. Additionally, the ACE conditioning stimulation inhibited the JOR induced by the stimulation of the sensory trigeminal nuclear complex in a similar manner, but not the jaw-opening response induced by the stimulation of the trigeminal motor nucleus (Mo V). Also, the conditioning stimulation influenced neither the evoked potentials induced by the tooth pulp stimulation at the main sensory and rostral nuclei nor the jaw-closing reflex induced by the stimulation of the mesencephalic trigeminal nucleus (Mes V). These results suggest that the excitation of the cell bodies in the ACE exerts an inhibitory modulation on the JOR with no effect on the non-nociceptive reflex such as the jaw-closing reflex at the level of Mo V.

The effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on the response of tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI) was investigated in cats anesthetized with N2O-O2 (2:1) and 0.5% halothane. The tooth pulp test stimulus was a single 30-450 microA rectangular pulse, and the conditioning stimuli of the ACE were trains of 33 pulses (300 microA) delivered at 330 Hz. The ACE conditioning stimulation markedly suppressed the response of the slow-type neurons with latencies of more than 20 ms without any effect on the discharges of fast-type TPD neurons and spontaneous discharges. This inhibition was 68.9 +/- 24.7% (mean +/- SD) of the control. These findings suggest that there are at least two pathways for the ascending pulpal (nociceptive) information to the SI, and that the ACE modulates the transmission of impulses in one of the pathways.

No abstract

The effect of stimulation of the entopeduncular nucleus (EP) on the jaw-opening reflex (JOR) was studied in the cat anesthetized with sodium pentobarbital. JOR was quantified by the digastric electromyogram. The conditioning stimulation (train of 33 pulses at 330 Hz, 0.5 ms duration, 50-400 microA) of the EP powerfully inhibited the JOR induced by the tooth pulp stimulation. Conditioning stimulation with 300 microA produced inhibition which continued approximately 400 ms from the cessation of the stimulation. The injection of monosodium glutamate into EP elicited inhibition of the JOR that lasted about 15 min. Additionally, the conditioning stimulation inhibited the JOR induced by the stimulation of trigeminal rostral and caudal nuclei in a similar manner but not jaw-opening response induced by the stimulation of the trigeminal motor nucleus. Therefore, it is possible that the excitation of the EP exerts inhibitory modulation of JOR at the motor nucleus rather than the trigeminal sensory nucleus.