Non-dopaminergic neurones of the reticular part of substantia nigra can gate static fusimotor action onto flexors in cat.

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Abstract
The effect on the fusimotor system of electrical stimulation of the reticular part of the substantia nigra or of the injection of the GABA antagonist picrotoxin into this structure was studied in spindle receptors of pretibial flexors in cats anesthetized with ketamine. Afferent activity of muscle spindle primary endings was recorded before and during these 2 forms of intranigral stimulation. Dynamic spindle sensitivity was assessed during both small- (l00 .mu.m) and large-amplitude (2 mm) sinusoidal stretching of the receptor-bearing muscles. From changes in spindle sensitivity after nigral electrical stimulation (11 of 14 primary endings) or intranigral injection of picrotoxin (51 of 67 primary endings) it is deduced that functional activation of neurons 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 .mu.g in 1 .mu.l), was reversed by a subsequent intranigral injection of the GABA-agonist muscimol (0.4 .mu.g in 1 .mu.l), but remained unchanged after subsequent intracaudate injections of haloperidol (12.5 .mu.g in 5 .mu.l) or apomorphine (5 .mu.g in 5 .mu.l). The CNS can gate static fusimotor action onto flexor muscle spindle primary endings through non-dopaminergic output neurons of the reticular part of substantia nigra.