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Journal of Neuroscience, Vol 7, 463-472, Copyright © 1987 by Society for Neuroscience

ARTICLE

Brain-stem perturbations during cortically evoked rhythmical jaw movements: effects of activation of brain-stem loci on jaw muscle cycle characteristics

SH Chandler and M Tal

The purpose of the present study was to further elucidate with the use of microstimulation techniques the influences of rostral pons and midbrain loci on the neuronal networks responsible for cortically induced rhythmical jaw movement (RJM) activity in the anesthetized guinea pig and to establish if these rostral brain-stem loci are capable of modulating the timing as well as the amplitude of rhythmical digastric (DIG) EMG activity. It was found that repetitive electrical stimulation of widespread areas of the rostral pons and mid-brain produced suppression of ongoing cortically induced rhythmical EMG activity. Prior to complete EMG suppression there was a reduction in amplitude of the DIG EMG and an increase in cycle duration. Repetitive stimulation of these suppressive loci also produced a reduction in the amplitude of the short-latency DIG EMG response produced by short pulse train stimulation of the masticatory cortex. This indicates that part of the suppression of cortically induced rhythmical EMG activity was due to a reduction in excitability of the polysynaptic short-latency pathway from cortex to DIG motoneurons. Short pulse train stimulation of these brain-stem suppressive loci during various phases of the rhythmical DIG cycle produced a phase-dependent increase in duration of the ongoing perturbed cycle. The cycles following the stimulus perturbation did not show any compensatory shortening in their durations suggesting that the stimulus produced a true resetting of the cycle. These data suggest that the brain-stem loci that produce suppression of RJMs evoked by repetitive cortical stimulation can affect the excitability of the central circuits responsible for cycle oscillation and timing as well as the excitability of the polysynaptic short-latency corticotrigeminal pathway to DIG motoneurons.

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