TY - JOUR
T1 - Primary afferent depolarization and presynaptic inhibition of monosynaptic group Ia EPSPs during posttetanic potentiation
AU - Lev-Tov, A.
AU - Fleshman, J. W.
AU - Burke, R. E.
PY - 1983
Y1 - 1983
N2 - In the pentobarbital-anesthetized cat, stimulation of group I afferents in the posterior biceps-semitendinosus (PBST) nerve produces the following effects: 1) decreases the amplitude of monosynaptic EPSPs from medial gastrocnemius (MG) group Ia afferents to medial gastrocnemius (MG) motoneurons, 2) increases the excitability of MG group Ia afferents, and 3) generates depolarizing transmembrane potentials in MG group Ia afferents. We have examined these effects of PBST conditioning before and after high-frequency tetanization of the group I afferents in the MG nerve. 2. Tetanization of MG group I afferents for 20 s at 500 Hz enhances the relative inhibition of MG Ia excitatory postsynaptic potentials (EPSPs) produced by group I volleys (4 shocks at 200 Hz) in the posterior biceps-semitendinosus (PBST) nerve. Relative EPSP inhibition was calculated as the ratio of conditioned to unconditioned responses obtained by alternating PBST-conditioned and unconditioned trials before and after the long MG nerve tetanus. Detailed examination of the shape of conditioned and unconditioned EPSPs indicated that the posttetanic increase in inhibition was not accounted for by changes in postsynaptic inhibitory conductances and the observed EPSP inhibition was attributed largely, if not exclusively, to presynaptic inhibition. 3. As expected, the excitability of MG Ia afferents to direct stimulation within the MG motor nucleus was increased when test stimuli were preceded by a conditioning train to PBST group I afferents. After tetanizing the MG group I afferents, the excitability of the MG Ia afferents without PBST conditioning was much reduced and returned to base-line values very slowly (>80 s). However, when conditioned by PBST stimulation, posttetanic MG Ia excitability quickly (<10 s) reached the same high levels found for pretetanic conditioned response. Thus, the relative group Ia excitability (the ratio of PBST-conditioned to unconditioned antidromic responses) was markedly enhanced after MG tetanization and this enhancement decayed slowly. 4. 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. 5. 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 1) that this PAD is generated by a conductance increase produced in Ia terminals by axoaxonic chemical synapses and 2) 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.
AB - In the pentobarbital-anesthetized cat, stimulation of group I afferents in the posterior biceps-semitendinosus (PBST) nerve produces the following effects: 1) decreases the amplitude of monosynaptic EPSPs from medial gastrocnemius (MG) group Ia afferents to medial gastrocnemius (MG) motoneurons, 2) increases the excitability of MG group Ia afferents, and 3) generates depolarizing transmembrane potentials in MG group Ia afferents. We have examined these effects of PBST conditioning before and after high-frequency tetanization of the group I afferents in the MG nerve. 2. Tetanization of MG group I afferents for 20 s at 500 Hz enhances the relative inhibition of MG Ia excitatory postsynaptic potentials (EPSPs) produced by group I volleys (4 shocks at 200 Hz) in the posterior biceps-semitendinosus (PBST) nerve. Relative EPSP inhibition was calculated as the ratio of conditioned to unconditioned responses obtained by alternating PBST-conditioned and unconditioned trials before and after the long MG nerve tetanus. Detailed examination of the shape of conditioned and unconditioned EPSPs indicated that the posttetanic increase in inhibition was not accounted for by changes in postsynaptic inhibitory conductances and the observed EPSP inhibition was attributed largely, if not exclusively, to presynaptic inhibition. 3. As expected, the excitability of MG Ia afferents to direct stimulation within the MG motor nucleus was increased when test stimuli were preceded by a conditioning train to PBST group I afferents. After tetanizing the MG group I afferents, the excitability of the MG Ia afferents without PBST conditioning was much reduced and returned to base-line values very slowly (>80 s). However, when conditioned by PBST stimulation, posttetanic MG Ia excitability quickly (<10 s) reached the same high levels found for pretetanic conditioned response. Thus, the relative group Ia excitability (the ratio of PBST-conditioned to unconditioned antidromic responses) was markedly enhanced after MG tetanization and this enhancement decayed slowly. 4. 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. 5. 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 1) that this PAD is generated by a conductance increase produced in Ia terminals by axoaxonic chemical synapses and 2) 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.
UR - http://www.scopus.com/inward/record.url?scp=0020963745&partnerID=8YFLogxK
U2 - 10.1152/jn.1983.50.2.413
DO - 10.1152/jn.1983.50.2.413
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C2 - 6310061
AN - SCOPUS:0020963745
SN - 0022-3077
VL - 50
SP - 413
EP - 427
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
IS - 2
ER -