1. We evoked steady-state synaptic potentials in triceps surae motoneu
rons of the cat by stimulating the hindlimb projection area of the con
tralateral magnocellular red nucleus at 200 Hz. We measured the effect
ive synaptic currents (I(N)) underlying the synaptic potentials using
a modified voltage-clamp technique. We also determined the effect of t
he rubrospinal input on the discharge rate of some of the motoneurons
by inducing repetitive discharge with long injected current pulses dur
ing which the red nucleus stimulation was repeated. 2. At motoneuron r
esting potential, the distribution of I(N) from the red nucleus within
the triceps surae pools was qualitatively similar to the distribution
of synaptic potentials: 86% of the putative type F motoneurons receiv
ed a net depolarizing I(N) from the red nucleus stimulation, whereas o
nly 38% of the putative type S units did so. The mean values of I(N) w
ere significantly different in the two groups [+4.1 +/- 5.0 nA (SD) fo
r putative type F and -1.6 +/- 3.1 nA for putative type S]. 3. However
, when the values of I(N) at threshold for repetitive firing were esti
mated, the distribution of I(N) from the red nucleus was quite differe
nt. At threshold, all of the putative type S units received hyperpolar
izing I(N) but so did nearly half of the putative type F units. 4. As
would be expected from the wide range of I(N) at threshold (-20 to +12
nA), the red nucleus input produced dramatically different effects on
the discharge of different motoneurons. The discharge rates of those
motoneurons that received depolarizing I(N) at threshold were accelera
ted by stimulating the red nucleus (+5 to +14 imp/s), whereas the disc
harge rates of cells that received hyperpolarizing currents were retar
ded by the rubrospinal input (-4 to -21 imp/s). 5. The red nucleus syn
aptic input reduced motoneuron input resistance by 40% on average. The
effect on input resistance was most pronounced in those motoneurons t
hat received hyperpolarizing I(N). 6. Our findings indicate that the r
ed nucleus input may provide a powerful source of synaptic drive to so
me high-threshold motoneurons while concurrently inhibiting low-thresh
old cells. Thus this input system can potentially alter the gain of th
e input-output function of the motoneuron pool as well as disrupt the
normal hierarchy of recruitment thresholds.