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We present evidence that the electrical excitability of the terminals of a group of spinal premotor interneurons can be increased after stimulation of sensory afferents. The interneurons were located in the midlumbar segments of the spinal cord and had projections to the lower lumbar motor nuclei. Thresholds for antidromic activation of a substantial number of interneurons were reduced after electrical stimulation of group II muscle afferents. Several observations suggest that the excitability changes are unlikely to have arisen from electrotonic spread of depolarization from the interneuron soma to its terminals or by environmental changes in the vicinity of the terminals related to neuronal activity. A particularly interesting possibility is that the excitability of the central terminals of the interneurons is increased because they are depolarized by a mechanism similar to that acting at the terminals of primary sensory afferents (primary afferent depolarization, PAD), which accompanies one type of presynaptic inhibition. This type of presynaptic action has been shown in premotor interneurons in the lamprey but not in the mammalian spinal cord. From our observations the organization of the systems generating excitability changes at the interneuron terminals seem in general to parallel the organization of the systems generating PAD at afferent terminals, raising the possibility that common principles might underlie the operation of this form of presynaptic control.

Evoked Excitability Changes at the Terminals of Midlumbar Premotor Interneurons in the Cat Spinal Cord