SYNAPTIC POTENTIALS OF MOTONEURONES

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Abstract
Motoneurones of the cat''s or frog''s spinal cord have been subjected to direct synaptic excitation by a single synchronous volley of impulses, and the resulting potential changes have been recorded from the ventral root fibres as they emerge from the spinal cord. When synaptic transmission of impulses is blocked by a sufficiently deep anesthesia, a negative potential change is still set up in the motoneurones and propagated electronically along the ventral root fibres. This catelectrotonic potential (called the synaptic potential) is shown to be homologous with the endplate potential of striated muscle and the synaptic potential of sympathetic ganglia. There is summation of synaptic potentials set up by 2 volleys or by repetitive stimulation. When synaptic transmission of single volleys is just blocked by anesthesia, a discharge is still produced by a second volley at a short interval[long dash]up to 15 msec, in the cat. The size and latent period of this facilitated response show the variation with stimulus interval that would be expected if facilitation were due to summation of the synaptic potentials. In the unanesthetized preparation, the synaptic potential begins at least 0.2 to 0.3 msec, before the discharge of impulses by the motoneurones and it appears that the synaptic potential is the sole causal factor in setting up the discharge of impulses from motoneurones. The anesthetic, nembutal, blocks transmission largely by increasing the stability of the membrane, but also partly by diminishing the production of synaptic potential. It has no appreciable action on the time course of the synaptic potential. Analysis of the synaptic potential by means of the local potential theory gives a short duration (2 msec, cat) for the synaptic transmitter action. No appreciable lengthening of this duration is observed after rapid repetitive stimulation, even after eserinization. This latter finding is considered in relationship with the evidence so far adduced that acetylcholine is the synaptic transmitter, and it is concluded that acetylcholine probably plays no significant role in synaptic transmission in the spinal cord. The evidence presented in this paper accords with the hydothesis that synaptic transmission in the spinal cord is due to the action currents of the pre-synaptic impulses.
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