The discharge of single α-motoneuron axons was recorded from small cut filaments of the medial gastrocnemius (MG) muscles nerve in the decerebrated cat preparation before and after a dorsal hemisection of the thoracic spinal cord. The remainder of the MG muscle nerve was left intact, and muscle force and multiunit electromyographic (EMG) activity were recorded along with α-motoneuron discharge, while motor output was varied by manual stimulation of the contralateral hindlimb. We recorded activity in 32 mononeurons before and after the spinal lesion, and pre- and postlesion recruitment forces and minimum firing rates were determined for 30 of these. Postlesion decreases in minimum firing rates were observed in 25/30 motoneurons, and decreases in recruitment force were seen in 21/30 motoneurons. The remaining motoneurons, which generally had low presection recruitment forces and minimum rates, exhibited postlesion increases in both parameters. The effects of the spinal lesion on the recruitment force and minimum firing rate of a motoneuron were related to the prelesion values of these parameters; the largest postlesion decreases were seen in motoneurons with the highest prelesion rates and recruitment forces. Spinal lesions thus acted to shift and compress the range of recruitment forces and minimum firing rates, so that after the lesion all motoneurons tended to exhibit discharge behavior typical of that seen only in the lowest motoneurons before the lesion. In addition, motoneurons with low prelesion recruitment forces (<1.0 N of active force) generally showed an increase in recruitment force after the lesion, indicating that the lesion may have led to changes in the prelesion recruitment order. Direct evidence of recruitment reversals was obtained in 4/14 experiments where two or more motoneurons were followed pre- and postlesion. The lesion-induced changes in motoneuron discharge characteristics were associated with changes in the relations between muscle force, rectified EMG, and motoneuron rate. Postlesion discharge rates were always significantly lower than the prelesion rates when compared over the same range of EMG levels. This postlesion drop in discharge rates was generally associated with inefficient force production, as evidenced by a significant drop in muscle force for matched EMG levels. The degree of discharge synchrony in MG motoneurons was assessed by calculating a spike-triggered average (STA) between axonal discharge and multiunit rectified EMG. Significant STA peaks were rare before the lesion (4/32 motoneurons) but were quite common after the lesion (29/32 motoneurons). In the four cases where significant peaks were present before the lesion, the magnitude of the peak showed a large increase after the lesion (from 1.8-3.8 times the prelesion value). Thus, while motoneuron discharge synchrony was either weak or absent before the lesion, both the degree of synchronization and its frequency of occurrence were greater after the lesion. Although the lesion-induced alterations in motoneuron discharge may have resulted in part from changes in transmission in certain segmental reflex pathways, we propose that the lesion also produces an acute change in the intrinsic membrane properties of α-motoneurons. Such a change could follow a reduction in the local concentration of some neuromodulator substance that normally regulates the magnitude or time course of a voltage-sensitive ionic conductance involved in repetitive discharge behavior.
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