ELECTRIC POTENTIALS GENERATED BY ANTIDROMIC VOLLEYS IN QUADRICEPS AND HAMSTRING MOTONEURONES

Abstract

Maximal antidromic volleys were fired into quadriceps or hamstring motoneurones, and the action potentials so generated have been recorded by an indifferent electrode and a micro-electrode. The micro-electrode was inserted by a micro-manipulator along a series of tracks lying in one transverse plane through the spinal cord and either through or adjacent to the motor nucleus. Information derived from the micro-manipulator and subsequent histological examination enabled transverse maps to be constructed, showing accurately each track and the positions along it at which antidromic potentials were recorded. An attempt was made to analyze such anti dromic potentials into that fraction generated by the antidromic impulse travelling in the motor axons and that attributable to antidromic invasion of the soma and dendrites. This analysis was largely based on the postulate (supported by all relevant exptl. evidence) that antidromic transmission is blocked at the axon-soma junctions of many motoneurones, such blockage occurring in more motoneurones during the depressive action of a conditioning antidromic volley, and in fewer during facilita tion by synaptic excitatory action. Hence the components of the antidromic potential revealed to be labile by such tests are attributable to antidromic invasion of the somas and dendrites, while the initial positive non-labile spike would be generated by the antidromic volley in the axons. Antidromic invasion of quadriceps motoneurones sets up a labile spike-like negativity of a micro-electrode lateral and ventral to the motor nucleus, while dorsal and medial there is an inverse potential. It is postulated that the dendrites are preponderantly distributed dorsally and medially, and that, when the antidromic impulse invades the soma and dendrites of a motoneurone, its propagation eventually fails towards the dendritic terminals, which consequently act as sources for the sinks on the soma and proximal dendrites. The axon also then acts as a source. On the contrary, antidromic invasion of hamstring motoneurones sets up currents largely flowing in "closed fields" almost as much as with the hypoglossal nucleus (Lorente de No.) With an intranuclear micro-electrode there is often a large labile positive potential during antidromic activation of the motoneurones. This is attributed to injured motoneurones and is shown to be produced by one or a few motoneurones very close to the micro-electrode. Investigations are described on such antidromic responses of single motoneurones. Consideration of the geometrical factors encountered in antidromic propagation provides an explanation of the blockage or delay at the axon-soma junction as well as of the postulated slowing and blockage towards the dendritic terminals. However, it apppears that the spike response of the soma and dendrites is at least 1 msec, in duration and hence about double that of the axon. This longer duration and the oscillatory activity show that, apart from geometrical differences, the excitatory properties of the soma and dendrites differ to some extent from those of the axon.