The effects of baclofen on the stretch reflex parameters of the cat

Experiments were done in cats decerebrated at the precollicular postmammillary level to determine how a tonic increase of presynaptic inhibition of the intraspinal terminals of muscle spindle afferents changes the mechanical properties of the soleus stretch reflex (s.r.). Baclofen, a specific GABAB receptor agonist, was injected i.v. (1–2 mg/kg) so as to induce a tonic increase in presynaptic inhibition. The effects of baclofen on the stiffness and threshold of the s.r. were determined, respectively, from plots of stiffness vs background force and force vs length (length-tension plot). Baclofen, at these doses, had no effect on the excitation-contraction coupling properties of muscle or on the intrinsic stiffness-force relation. Changes of the soleus background force, required to obtain the stiffness vs force plots, were produced by stimulation of the contralateral common peroneal nerve or the posterior tibial nerve and occasionally by electrical stimulation in the area of the red nucleus. The stiffness of the s.r. as a function of the background force level was determined by stretching the muscle with a square pulse of 1–2 mm amplitude and 200–300 ms duration. The stiffness at each force level was calculated by dividing the change in force by the change in length, at a point where the force trace had stabilized. The length-tension relation of the s.r. was determined by stretching the muscle 12–17 mm at a constant rate of 1–2 mm/s. At all force levels, baclofen produced a significant decrease (40% or more) in the s.r. stiffness, within 10–15 min of injection as determined from the stiffness-force plots. The length-tension plots revealed that the decrease of s.r. stiffness was always accompanied by an increase in the s.r. threshold (typically 2–3 mm). It is suggested, therefore, that the s.r. threshold is not an independent variable, depending on the membrane potential of the α- motoneurons, and additionally on the level of presynaptic inhibition of the muscle spindle afferent terminals. The present results also imply that it may be possible for the CNS to adaptively modify the s.r. stiffness via presynaptic inhibition of the intraspinal terminals of muscle afferents. However, any such change of s.r. stiffness will be accompanied by a change in the s.r. threshold.