Mechanisms of post‐synaptic excitation in amphibian motoneurones.

Abstract

Post-synaptic excitation produced in motoneurons of the isolated perfused frog (Rana ridibunda) spinal cord by different monosynaptic inputs and by ionophoretically applied glutamate was analyzed with an intracellular recording technique. Ca2+-deficient, high Mg2+ (5-20 mM) media or addition of Mn2+ (2 mM) or Co2+ (5 mM) reversibly abolished chemically mediated EPSP [excitatory post-synaptic potential] derived from medullary reticular formation, ventral and lateral columns, but not the short-latency, rapidly rising EPSP derived from dorsal roots or muscle nerves, suggesting electric coupling between some primary afferents and spinal motoneurons. This conclusion is consistent with the dynamic properties of dorsal root EPSP, their small sensitivity to cooling, and with results of correction of intracellular records made for contribution of extracellular field potential. EPSP evoked by ventral root stimulation was also insensitive to Ca2+-lack and presence of 5-10 mM-Mg2+. As the post-synaptic membrane was made more negative the amplitude of electrotonic dorsal root EPSP was increased, and it was decreased by depolarizing currents. No reversal of the early part of the electrotonic EPSP was observed. When hyperpolarizing and depolarizing currents were applied to motoneurons in which chemically mediated EPSP of the reticular cells, the ventral and lateral columns, were evoked, the actual reversal of the early part of EPSP was not observed, and there was no correlation between the sensitivity of the EPSP to injected currents and their time course. The positive values of the extrapolated reversal potentials and the effects of changes in ionic content of perfusing media suggest that synaptically released transmitter triggers off the Na permeability of the subsynaptic membrane. The amplitude of depolarization produced by ionophoretically applied glutamate depends non-linearly on membrane potential and the curvature of this dependence differs from that seen with chemically mediated EPSP. The asymptotic nature of this relationship is explicable by a dependence of the membrane conductance change upon the membrane voltage. The results of conductance measurements during the glutamate induced depolarization, the values of apparent reversal potentials and their dependence on external Na+ and K+ and internal Cl- is explicable by the opening post-synaptic channel gates for Na+ and closing post-synaptic channel gates for K+. Chemical and electrical transmission in the amphibian cord is discussed in relation to recent anatomical findings.