On the origin of presynaptic depolarization of group I muscle afferents in Clarke's column in the cat.

The origin of presynaptic depolarization of group I afferents in Clarke's column has been re-investigated, using changes in excitability of single fibres as a measure of their depolarization. In contrast to the previously reported lack of effects following conditioning stimulation of group Ia afferents, these afferents have been found to increase the excitability of other group Ia afferent terminals in Clarke's column. Flexor Ia and Ib afferents were found to be more effective than extensor afferents. The group I origin of the presynaptic depolarization of group I afferents in Clarke's column thus appears to be as of other terminals of these afferents. In order to define the location of interneurones mediating primary afferent depolarization in Clarke's column, changes in the excitability of afferents in Clarke's column were measured after isolating L4 and more rostral segments from the sacral and caudal lumbar segments, except for the dorsal columns, or after transection of ipsilateral lateral and ventral funiculi. Primary afferent depolarization of group Ia, or unspecified group I origin, was also found after such lesions and its effectiveness appeared to be as in intact preparations. It may thus be evoked primarily by interneurones located in the same segments as Clarke's column.