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The effect on the fusimotor system of electrical stimulation of the reticular part of the substantia nigra or of the injection of the gamma-aminobutyric acid (GABA)-antagonist picrotoxin into this structure was studied in spindle receptors of pretibial flexors in cats anaesthetized with ketamine. Afferent activity of muscle spindle primary endings was recorded before and during these two forms of intranigral stimulation. Dynamic spindle sensitivity was assessed during both small- (100 microns) and large-amplitude (2 mm) sinusoidal stretching of the receptor-bearing muscles. From changes in spindle sensitivity after nigral electrical stimulation (eleven out of fourteen primary endings) or intranigral injection of picrotoxin (fifty-one out of sixty-seven primary endings) it is deduced that functional activation of neurones of the reticular part of substantia nigra, in this preparation, removed a normally present tonic static fusimotor action from the primary sensory endings of pretibial flexor muscle spindles. This effect, induced by picrotoxin (2 micrograms in 1 microliter), was reversed by a subsequent intranigral injection of the GABA-agonist muscimol (0.4 microgram in 1 microliters), but remained unchanged after subsequent intracaudate injections of haloperidol (12.5 micrograms in 5 microliters) or apomorphine (5 micrograms in 5 microliters). It is concluded that the C.N.S. can gate static fusimotor action onto flexor muscle spindle primary endings through non-dopaminergic output neurones of the reticular part of substantia nigra.