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This study was aimed at elucidating the brainstem-spinal mechanisms of postural suppression evoked by stimulating the dorsal portion of the caudal tegmental field (DTP) in the pons. For this purpose, we first sampled a group of reticulospinal neurons located in the medial part of medullary reticular formation, which were activated ortho-dromically and antidromically by stimulating the DTF area and the first lumbar spinal segment, respectively (DTF-RS neurons; N = 26). These DTF-RS neurons were located within the nucleus reticularis gigantocellularis (NRGc) and projected their descending axons to the lumbar spinal cord through the ventrolateral funiculus. The postsynaptic inhibitory effects of single DTF-RS neurons upon hindlimb alpha-MNs intracellularly recorded (N = 78) were then studied with spike-triggered averaging. Twelve DTF-RS neurons evoked IPSPs in 21 hindlimb alpha-MNs. Five DTF-RS neurons exerted postsynaptic inhibitory effects upon more than one alpha-MNs. These alpha-MNs were located from L5 to S1 segments of the spinal cord. A mean latency of IPSPs which was measured from the onset of the trigger spike was 5.1 ms with time to peak of 1.8 ms, and the mean segmental delay of the IPSPs was 1.5 ms, which was measured from the onset of the descending axonal volley recorded extracellularly adjacent to alpha-MNs. Amplitudes of the IPSPs were augmented with an increase in the firing frequencies of the DTF-RS neurons, the increase being produced by iontophoretic application of glutamate. These characteristics of the IPSPs suggest that reticular effects are mediated at least by a single spinal inhibitory interneuron. These results suggest that the DTF-NRGc system participates in generalized motor inhibition.

We have previously defined three types of tegmental pedunculopontine nuclei neurons based on their electrophysiological characteristics: Type I neurons characterized by low-threshold Ca2+spikes, Type II neurons which displayed a transient outward current (A-current), and Type III neurons having neither low-threshold spikes nor A-current [Kang Y. and Kitai S. T. (1990) Brain Res. 535,79–95]. In this report, ionic mechanisms underlying repetitive firing of Type I (n=15) and Type II (n=69) neurons were studied in in vitroslice preparations. Type I neurons did not fire rhythmically but their spontaneous firing frequency ranged from 0 to 19.5spikes/s (mean 9.7spikes/s). The spontaneous firing of Type II neurons was rhythmic, with a mean frequency of 9.6spikes/s (range 3.5–16.0spikes/s). Choline acetyltransferase immunohistochemistry combined with biocytin labeling indicated that none of the Type I neurons were immunopositive to choline acetyltransferase, while 60% (42 of 69) of Type II neurons were immunopositive. There was no apparent difference in the electrophysiological membrane properties of immunopositive and immunonegative Type II neurons. At membrane potentials subthreshold for Na+spikes (−50mV), spontaneous membrane oscillations (11.6Hz) were observed: these underlie the spontaneous repetitive firing of Type I neurons. The subthreshold membrane oscillation was tetrodotoxin sensitive but was not affected by Ca2+-free medium. A similar tetrodotoxin-sensitive subthreshold membrane oscillation (10.5Hz) was also observed in Type II neurons. However, in Type II neurons a membrane oscillation was also observed at higher membrane potentials (>−50mV). This high-threshold oscillation was insensitive to tetrodotoxin and Na+-free medium, but was eliminated in Ca2+-free conditions. The amplitude and frequency of the high-threshold oscillation was increased upon membrane depolarization. At the most prominent oscillatory level (around −40mV), the high-threshold oscillation had a mean frequency of 8.8Hz. The high-threshold Ca2+spike was triggered from the peak potential (−35 to −30mV) of the high-threshold oscillation. Application of tetraethylammonium chloride (<5mM) increased the amplitude of the high-threshold oscillation, while nifedipine greatly attenuated the high-threshold oscillation without changing the shape of the high-threshold Ca2+spike. Application of Cd2+eliminated both the high-threshold oscillation and the high-threshold Ca2+spike, and ω-conotoxin reduced the size of the high-threshold Ca2+spike without affecting the frequency of the high-threshold oscillation. Nickel did not have any effect on either the high-threshold oscillation or the high-threshold Ca2+spike.