Alterations in motoneuron properties induced by acute dorsal spinal hemisection in the decerebrate cat.

Using intracellular recording techniques, we studied the response characteristics of two separate populations of triceps surae motoneurons in unanesthetized decerebrate cats, recorded before and after low thoracic hemisection of the spinal cord. In each preparation, we studied the response properties of one group of motoneurons and the protocol was then repeated for a separate group, immediately following the dorsal hemisection. In each group, we examined both the minimum firing rates of motoneurons during intracellular current injection and a range of cellular properties, including input resistance, rheobase current and afterhyperpolarization time course and magnitude. Although earlier studies from this laboratory have shown substantial reductions in minimum firing rate in reflexively active motoneurons in the hemisected decerebrated preparation, the response of motoneurons to intracellular current injection in the current preparation proved to be quite different. Minimum firing rates were either normal or even somewhat higher in the post-lesion group, while the time course of the afterhyperpolarization was shortened. Moreover, these effects were not evenly distributed across the motoneuron pool. The rate effect was most evident in motoneurons with higher conduction velocity, while the afterhyperpolarization effect occurred predominantly in motoneurons with lower conduction velocity. Neither of these effects could be accounted for by lesion-induced changes in other cellular properties. We conclude that tonically active neurons with descending axons traversing dorsolateral white matter may influence both the discharge characteristics and membrane properties of spinal motoneurons in novel ways, presumably by modifying voltage or calcium activated motoneuronal conductances. The previously described reactions in the firing rate of motoneurons after such lesions appear to be mediated by different means, perhaps by alterations in synaptic input from segmental interneurons.