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* To whom correspondence should be addressed. E-mail: serge.rossignol{at}umontreal.ca.
In acute experiments performed in decerebrated and spinalized (T13) cats (Marcoux and Rossignol 2000), an intraspinal injection of clonidine, a noradrenergic agonist, restricted to mid-lumbar segments L3-L4, can induce hindlimb locomotion while yohimbine, a noradrenergic antagonist, can block spinal locomotion while a second spinal lesion at L4 can abolish all locomotor activity. In the present study, we investigated whether the abolition of locomotion after this second spinal lesion was due to an acute spinal shock or to the functional disconnection of the rostral and caudal lumbar segments. In 7 cats, first spinalized at T13 and having recovered treadmill locomotion, a second transection was performed at lower lumbar levels. Video and electromyographic recordings were used to evaluate locomotor performance. Results show that 1) after a second transection at L2 or rostral L3 levels, spinal locomotion was maintained; 2) when the second lesion was performed at caudal L3 or L4, all locomotor activity was abolished, even after several weeks of attempted locomotor training; 3) vigorous fast paw shakes (FPS) were observed in all cases; 4) after an i.p. injection of clonidine in cats with a second transection at L3-L5, perineal stimulation induced hyperextension of the hindlimbs but no locomotion. Considering that the main motoneurone pools of the hindlimbs are caudal to L4 and are still functional after the second spinal transection, as evidenced by the presence of FPS, we conclude that the mid-lumbar spinal segments are essential for the specific expression of spinal locomotion but not necessarily for other rhythmic motor patterns.
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