Modulation of responses of feline γ-motoneurones by noradrenaline, tizanidine and clonidine

1. Effects of noradrenaline (NA) and the alpha(2) agonists tizanidine and clonidine were tested on extracellularly recorded responses of gamma-motoneurones in deeply anaesthetized cats. Two types of responses were used; firstly, short latency phasic responses evoked by electrical stimulation of group II afferents in a muscle nerve and, secondly tonic background discharges. 2. Responses evoked by group II muscle afferents were depressed when NA and tizanidine were applied ionophoretically close to a gamma-motoneurone and when clonidine was applied systemically. The number of spike potentials evoked by stimulation of these afferents decreased and their latencies increased. Responses evoked by flexor or extensor afferents in gamma-motoneurones innervating flexors or extensors were similarly depressed. 3. Tonic discharges were inconsistently and/or insignificantly affected by locally applied NA and tizanidine but were depressed by systemically applied clonidine. 4. Control tests indicate specific effects of NA and tizanidine application since similarly ionophoresed H+ ions did not change responses of gamma-motoneurones to stimulation of group II afferents, or only weakly enhanced their background discharges. Furthermore, serotonin ejected from a solution with a similar pH facilitated rather than depressed responses of gamma-motoneurones. 5. The results indicate that some antispastic effects of clonidine and tizanidine may be due to the depression of group II-evoked responses of gamma-motoneurones, resulting in weaker responses of muscle spindles to muscle stretches.