Primary afferent de polarization and presynaptic inhibition of mono synaptic group ia excitatory postsynaptic potentials during post tetanic potentiation

Lev Tov, A.; Fleshman, J.W.; Burke, R.E.

Journal of Neurophysiology (Bethesda) 50(2): 413-427


Accession: 006182055

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In the pentobarbital-anesthetized cat, stimulation of group I afferents in the posterior biceps-semitendinosus (PBST) nerve produces the following effects: decreases the amplitude of monosynaptic EPSP from medial gastrocnemius (MG) group Ia afferents to (MG) motoneurons, increases the excitability of MG group Ia afferents, and generates depolarizing transmembrane potentials in MG group Ia afferents. The effects of PBST conditioning were examined before and after high-frequency tetanizing of the group I afferents in the MG nerve. Tetanization of MG group I afferents for 20 s at 500 Hz enhances the relative inhibition of MG Ia EPSP produced by group I volleys (4 shocks at 200 Hz) in the PBST nerve. Relative EPSP inhibition was calculated as the ratio of conditioned to unconditioned responses obtained by alternating PBST-conditioning and unconditioned trials before and after the long MG nerve tetanus. Detailed examination of the shape of conditioned and unconditioned EPSP indicated that the posttetanic increase in postsynaptic inhibitory conductances and the observed EPSP inhibition was attributed largely, if not exclusively, to presynaptic inhibition. Primary afferent depolarization (PAD) produced by PBST conditioning volleys were recorded in functionally identified MG Ia afferents in the dorsal column. MG tetanization produced tonic hyperpolarization in Ia afferents and marked enhancement of the phasic PAD generated by PBST volleys. In addition, PAD time to peak was prolonged in the posttetanic period and the depolarizing responses were cut short by the development of a hyperpolarizing undershoot, which disappeared more rapidly than the enhancement of peak PAD. The time courses of posttetanic changes in relative group Ia EPSP inhibition, MG Ia afferent excitability, and phasic PAD enhancement in MG Ia afferents were all strikingly similar. These observations are most simply explained by assuming that this PAD is generated by a conductance increase produced in Ia terminals by axoaxonomic chemical synapses and that the posttetanic enhancement in indices of PAD and in Ia EPSP inhibition are due to the transmembrane hyperpolarization that develops when afferent fibers are tetanized. The results are consistent with the hypothesis that PAD causes presynaptic inhibition.