ROLES OF DEITER'S NEURONS DURING POSTURAL DISTURBANCES IN THE REFLEX STANDING DECEREBRATE CATS

Abstract

In this study, an attempt was made to understand functional roles of Deiter's neurons (cells of origin contributing to the vestibulo-spinal tract) for postural control. The acute precollicularpostmammillary decerebrate cats which were maintained in a reflex standing posture with or without external support were employed. During standing, the force exerted by each of the hindlimbs was measured by a force transducer placed underneath the foot along with the electromyographic activities of hindlimb extensor muscles. The force and the EMGs were considered to represent the degree of hindlimb muscle tone. To perturb standing posture, the dorsal portion of the caudal tegmental field in the pons was selectively stimulated by means of a microelectrode. The stimuli consisted of pulse trains (duration 0.2ms; frequency 50 pulses/s) lasting 5s at intensities ranging from 20 to 60μA. Such stimuli decreased the tone of the hindlimb muscles. The decrease in the force and tonic discharges of extensor muscles increased with an increase in stimulus intensity, and persised even after termination of the stimulation. During this period the cat was able to maintain standing posture only with the aid of external support.
Deiter's neurons (n=62) discharged tonically during reflex standing of the cat. There were, however, no significant relation between the firing frequency of neurons and the level of hindlimb muscle tone. During postural disturbance, most Deiter's neurons (n=54) increased their firing frequencies. The faster and the larger were the force decrease, the greater the phasic increase in the firing frequencies of neurons. Furthermore, time to the maximum firing freqencies of Deiter's neurons tended to be shorten with an increase in the decreasing rate of the hindlimb forces. During immobilization of decerebrate cats, such phasic increases in the firing frequencies were not consistently observed but the tonic increases of them remained. All these results indicate that two different neuronal mechanisms underly the increase in the firing frequencies of Deiter's neurons. One is peripheral or feedback excitation resulting in the phasic increase in the firing frequencies of Deiter's neurons, and the other is the central or feedforward excitation resulting in the tonic and the phasic increases of them possibly by pathways within the brain stem. Based on these results, it can be concluded that Deiter's neurons play an important role for compensating centrally induced postural disturbances.