Interneurones mediating presynaptic inhibition of group II muscle afferents in the cat spinal cord.

1. To investigate whether dorsal horn interneurones with input from group II muscle afferents induce depolarization of sensory fibres, simultaneous recordings were made from single interneurones in the sacral segments and from sacral dorsal root filaments using the spike-triggered averaging technique. 2. The spike potentials of eighteen out of thirty-eight interneurones tested were followed by dorsal root potentials (DRPs). The DRPs occurred at latencies of 2 and 6-8 ms. Interneurones evoking DRPs at latencies of up to 2 ms are considered likely to be last-order interneurones in pathways of presynaptic inhibition, while those inducing DRPs at longer latencies are considered likely to be first-order interneurones. The former were activated by peripheral afferents with somewhat longer latencies than the latter. However, all interneurones were co-activated by group II muscle and cutaneous afferents, indicating that the depolarization of group II muscle afferents, which these afferents induce, may be mediated by the same interneurones. 3. DRPs evoked by electrical stimulation of peripheral nerves were recorded from both sacral and midlumbar dorsal root filaments. The amplitudes of these DRPs were closely related to the potency with which group II afferents of various nerves activate dorsal horn interneurones in the sacral and midlumbar segments and group II afferents contributed to them more effectively than group I afferents. The second stimulus in a train was more effective than the first, while a third stimulus had little additional effect, indicating that the interneurones involved are relatively easily activated. 4. Intraspinal stimuli applied within the dorsal horn, at the sites where the largest field potentials of group II origin were recorded, evoked distinct DRPs. However, the location of the first- and last-order interneurones in pathways of primary afferent depolarization (PAD) could not be differentiated by this approach because the same stimuli induced positive potentials, which masked the onset of DRPs and precluded localization of the sites from which DRPs might be evoked monosynaptically.