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Biomedical subjects

B I Shiriaev

Publications and source records attributed to B I Shiriaev.

31 records · Page 2Linked to original sources

Electrical coupling between primary afferents and amphibian motoneurons.

The short-latency DR-EPSPs resistant to Ca2+-lack and to addition of Mn2+ and Mg2+ result from electrical coupling between primary afferents and spinal motoneurons in frogs and toads. There are two time constants by which the time constant for the decay of the electronic DR-EPSP can be described: 1. the membrane time constant which determines the rate of passive decay of the membrane potential shift produced directly by the presynaptic spike, 2. the rate at which the presynaptic after-depolarization (ADP) declines. The latter value is very large as compared with the postsynaptic membrane time constant. Presynaptic tetanization does not change the magnitude of the initial spike-induced component of the EPSP but its later slowly decaying portion is potentiated markedly as a result of the post-tetanic increase in the amplitude of the ADP. The perfusion with substances blocking potential dependent potassium channels (4-AP and TEA) greatly augments the DR-EPSP due to prolongation of the presynaptic spike and appearance of multiple discharges in the presynaptic fibers. An antidromic electrical coupling between motoneurons and the terminals of primary afferents was demonstrated in the isolated amphibian spinal cord perfused with zero Ca2+, 2 mM Mn2+ solution containing TEA or 4-AP. Under these conditions ventral root volleys may evoke local graded depolarizing potentials in some sensory fibers. Such antidromic coupling potentials can reach the critical level for generating a single or multiple discharge.

Afferent Pathways↗

Two types of electronic EPSP evoked in amphibian motoneurons by ventral root stimulation.

Motoneurons of hemisected perfused frog spinal cord were used for intracellular recording of EPSP produced by ventral root stimulation. Two varieties of electrotonic VR-EPSP resistant to Ca-lack and to addition of 10 mM Mg2+ and 2 mM Mn2+ have been encountered. The early VR-EPSP started before the full somadendritic invasion and the time constant of their decay varied between 11 and 25 msec, mean 15.4 +/- 1.8 msec, i.e., it was significantly longer than the time constant of the motoneuronal membrane (2.6--6.9 msec, mean 4.4 +/- 0.5 msec). The late VR-EPSPs appeared after a latent period which was significantly longer than that of an antidromic spike. They started after the full somadendritic invasion and had very rapid time course, the time constant of their decay approximated that of the motoneuronal membrane. The shape of the late VR-EPSP both before and after treatment with 4-AP of TEA which markedly facilitated its appearance resembled the shape of an antidromic spike, whereas this correlation was not found in the case of the early VR-EPSP. When the temperature was elevated above 18--19 degree C the late VR-EPSPs disappeared but the early VR-EPSPs still could be recorded. The available evidence suggests that the early VR-EPSPs are produced by direct synaptic interconnections between motoneurons and recurrent collaterals of the motor axons, and the VR-EPSPs are transmitted across dendrodendritic junctions.

Aminopyridines↗

Modulation of transmission in different electronic junctions by aminopyridine.

4 distinct electronic inputs can be identified in amphibian motoneurons perfused with calcium-free solution containing manganese. The differential effect of 4-aminopyridine on different electronic junctions may reflect the peculiarities of molecular architecture of potassium channels in different electrically excitable presynaptic membranes.

Action Potentials↗

Mechanisms of post-synaptic excitation in amphibian motoneurones.

1. Post-synaptic excitation produced in motoneurones of the isolated perfused frog spinal cord by different monosynaptic inputs and by ionophoretically applied glutamate was analysed with intracellular recording technique. 2. Ca2+-deficient, high Mg2+ (5--20 mM) media or addition of Mn2+ (2mM) or Co2+ (5 mM) reversibly abolished chemically mediated e.p.s.p.s derived from medullary reticular formation, ventral and lateral columns, but not the short-latency, rapidly rising e.p.s.p.s derived from dorsal roots or muscle nerves, suggesting electric coupling between some primary afferents and spinal motoneurones. This conclusion is consistent with the dynamic properties of dorsal root e.p.s.p.s, their small sensitivity to cooling, and with results of correction of intracellular records made for contribution of extracellular field potential. E.p.s.p.s evoked by ventral root stimulation were also insensitive to Ca2+-lack and presence of 5--10 mM-Mg2+. 3. As the post-synaptic membrane was made more negative the amplitude of electrotonic dorsal root e.p.s.p.s was increased, and it was decreased by depolarizing currents. No reversal of the early part of the electrotonic e.p.s.p. was observed, although the presence of the local response would account for the occasional reversal of its later phase seen with depolarization. 4. When hyperpolarizing and depolarizing currents were applied to motoneurones in which chemically mediated e.p.s.p.s of the reticular cells, the ventral and lateral columns, were evoked, the actual reversal of the early part of e.p.s.p. was not observed, and there was no correlation between the sensitivity of the e.p.s.p.s 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. 5. 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 s.p.s.p.s. The asymptotic nature of this relationship is explicable by a dependence of the membrane conductance change upon the membrane voltage. 6. 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+. 7. Chemical and electrical transmission in the amphibian cord is discussed in relation to recent anatomical findings.

Animals↗

[Electrotonic transmission between primary afferent fibers and the motor neurons of the isolated spinal cord of various representative amphibians].

Studies have been made of monosynaptic excitatory postsynaptic potentials elicited by stimulation of the posterior root in motoneurones of the isolated spinal cord of the frog Rana ridibunda, toad Bufo bufo, and clawed toad Xenopus laevis. In all the amphibians studied, the early component of monosynaptic EPSP was not blocked in Ca-free medium containing 2 mM Mn2+. It is suggested that electrical coupling in anuran amphibians reflects certain stage of evolution of the synaptic transmission in vertebrates.

Afferent Pathways↗