title: The effects of lesions on autogenetic inhibition in the decerebrate cat.
abstract: 1. The effects of spinal and brain lesions on autogenetic inhibition from contraction receptors were studied in the decerebrate cat. Inhibitory feedback gain was estimated by measuring the effect of tension perturbations on reflex contractions of the soleus muscle. Tendon vibration was used to clamp the firing rate of primary spindle afferents, to prevent spindle unloading from disfacilitating the reflex contraction. In addition, secondary spindle afferents could be selectively excited by stimulating fusimotor fibres during muscle vibration. 2. Following an acute contralateral or bilateral dorsal transection of the spinal cord at L3, the vibration reflex tension fell by between 50 and 74% in three decerebrate animals. This was accompanied by a variable increase in inhibitory feedback, ranging between 180 and 360%. 3. In two animals, selective stimulation of fusimotor fibres supplying soleus muscle was without effect in the presence of muscle vibration both before and after the spinal lesion. In the third animal, a small and variable reduction in tension could be obtained only after the lesion, implying that an inhibitory pathway from homonymous secondary spindle afferents to alpha-motoneurones was released. 4. In a separate series of experiments, contralateral cerebral lesions were made 2-12 months prior to the acute inhibitory feedback measurement. Inhibitory feedback gain was increased, on average twofold in decerebrate animals with chronic cerebral lesions, when compared to control decerebrate animals. 5. Selective stimulation of fusimotor fibres to excite spindle secondary afferents was uniformly without effect in decerebrate animals with chronic cerebral lesions. In one animal spinal transection had only a minor effect on extensor tone and on inhibitory feedback gain, in contrast to the control decerebrate cats. 6. The implications of these findings are discussed in relation to the use of animals with spinal and supraspinal lesions as models of spasticity.
authors.affiliation: University Laboratory of Physiology, Oxford.
authors.forename: J F
authors.initials: JF
authors.lastname: Iles
authors.forename: J J
authors.initials: JJ
authors.lastname: Jack
authors.forename: D M
authors.initials: DM
authors.lastname: Kullmann
authors.forename: R C
authors.initials: RC
authors.lastname: Roberts
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000503:physiopathology*; D002415:Cats; D002818:Cordotomy; D003655:Decerebrate State / Q000503:physiopathology*; D005246:Feedback; D008465:Mechanoreceptors / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology*