Abstract
Forty functionally single gamma-efferents (20-42 m/s) to the triceps surae were isolated in ventral root filaments of the decerebrated and paralysed cat in order to study the effects of group I muscle afferents on their own fusimotor neurones. All the efferents studied were spontaneously active. During splitting the continuity of the efferent fibre was preserved so that the destination of the target muscle of the efferent could be determined by antidromic stimulation of the muscle nerve using the collision block technique. Thereafter the filament was cut so that the reflex response, uncontaminated by antidromic impulse invasion, could be recorded from the central end. Sixteen of forty gamma-efferents to the triceps were inhibited by repetitive stimulation (range -3 to -40 impulses/s) of the homonymous nerve within the group I range. Raising the stimulus strength above the group II threshold produced no further increase in inhibition. Twelve of these sixteen cells were also tested by stretching the triceps; ten showed marked inhibition, and two were not influenced. In ten of the sixteen inhibited cells, the autogenetic inhibition at maximum group I stimulus strength was larger than the maximum antidromic inhibition elicited by stimulation of the remainder of the cut ventral roots L7 and S1. Since both effects were additive, it is concluded that Renshaw inhibition is at least not solely responsible for the autogenetic inhibition. Consistent with this assumption is the observation that some cells receiving electrically evoked autogenetic inhibition were not susceptible to inhibition induced by small-amplitude vibration of the triceps. Since small-amplitude vibration is known to excite most of the Ia afferents of the vibrated triceps, Ib afferents must be involved in the autogenetic fusimotor inhibition. A contribution of Ia afferents to the autogenetic inhibition (via alpha-motoneurones and Renshaw cells or via Ib inhibitory interneurones) seems likely since inhibition, induced by small-amplitude vibration, was detectable in many of the cells receiving autogenetic group I inhibition. All of these cells were susceptible to antidromic inhibition. Ten of the forty cells tested responded with tonic facilitation to the homonymous nerve stimulation. Some arguments favour the view that static gamma-motoneurones are involved in the low-threshold autogenetic inhibition. The results strongly support earlier work suggest a regulatory function of low-threshold muscle receptors on their own gamma-motoneurones.