TY - JOUR
T1 - Posttetanic potentiation of group Ia EPSPs
T2 - Possible mechanisms for differential distribution among medial gastrocnemius motoneurons
AU - Lev-Tov, A.
AU - Pinter, M. J.
AU - Burke, R. E.
PY - 1983
Y1 - 1983
N2 - We have reinvestigated the phenomenon of posttetanic potentiation (PTP) of group I monosynaptic excitatory postsynaptic potentials (EPSPs) in medial gastrocnemius (MG) α-motoneurons of pentobarbital-anesthetized cats. The results generally confirm earlier reports by Luscher and colleagues of a negative correlation between the maximum percentage potentiation of Ia EPSP amplitude (P(max)) and 1) the mean amplitude of the pretetanic control EPSp in the same cell and 2) the input resistance of the postsynaptic motoneuron. These negative correlations, which we will refer to as 'differential distribution of PTP' within the MG motor pool, were less strong in the present work than reported by Luscher et al. We also found a relatively strong negative correlation between posttetanic EPSP depression, assessed by the amplitude of the first posttetanic EPSP, and the level of P(max) subsequently attained. We found no evidence that posttetanic depression is caused by failure of presynaptic action potentials. We investigated a second type of depression, referred to as 'specific' synaptic depression, in which the second EPSP of paired responses (interval 250 ms) is, on average, smaller in peak amplitude than the first EPSP. This phenomenon appears to reflect decreases in the probability of transmitter release from previously activated synapses. Specific synaptic depression was consistently increased when paired responses were conditioned by a high-frequency tetanus. This is most easily explained by postulating that PTP results, at least in part, from an increase in the statistical probability of transmitter liberation from group Ia synapses that are activated (i.e., presumably invaded by action potentials) both before and after afferent tetanization. On the basis of the present results and other available evidence, we conclude that the differential distribution of PTP can be explained by two main factors: 1) the non-linear relation between conductance and voltage changes inherent in all chemical synapses and 2) systematic variations in the properties of group Ia synapses that innervated different motoneurons, which remain to be clarified.
AB - We have reinvestigated the phenomenon of posttetanic potentiation (PTP) of group I monosynaptic excitatory postsynaptic potentials (EPSPs) in medial gastrocnemius (MG) α-motoneurons of pentobarbital-anesthetized cats. The results generally confirm earlier reports by Luscher and colleagues of a negative correlation between the maximum percentage potentiation of Ia EPSP amplitude (P(max)) and 1) the mean amplitude of the pretetanic control EPSp in the same cell and 2) the input resistance of the postsynaptic motoneuron. These negative correlations, which we will refer to as 'differential distribution of PTP' within the MG motor pool, were less strong in the present work than reported by Luscher et al. We also found a relatively strong negative correlation between posttetanic EPSP depression, assessed by the amplitude of the first posttetanic EPSP, and the level of P(max) subsequently attained. We found no evidence that posttetanic depression is caused by failure of presynaptic action potentials. We investigated a second type of depression, referred to as 'specific' synaptic depression, in which the second EPSP of paired responses (interval 250 ms) is, on average, smaller in peak amplitude than the first EPSP. This phenomenon appears to reflect decreases in the probability of transmitter release from previously activated synapses. Specific synaptic depression was consistently increased when paired responses were conditioned by a high-frequency tetanus. This is most easily explained by postulating that PTP results, at least in part, from an increase in the statistical probability of transmitter liberation from group Ia synapses that are activated (i.e., presumably invaded by action potentials) both before and after afferent tetanization. On the basis of the present results and other available evidence, we conclude that the differential distribution of PTP can be explained by two main factors: 1) the non-linear relation between conductance and voltage changes inherent in all chemical synapses and 2) systematic variations in the properties of group Ia synapses that innervated different motoneurons, which remain to be clarified.
UR - http://www.scopus.com/inward/record.url?scp=0020516164&partnerID=8YFLogxK
U2 - 10.1152/jn.1983.50.2.379
DO - 10.1152/jn.1983.50.2.379
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 6310059
AN - SCOPUS:0020516164
SN - 0022-3077
VL - 50
SP - 379
EP - 398
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
IS - 2
ER -