Abstract

The action potential of afferent terminals was recorded with microcapillary electrodes placed in the ventral gray matter of the spinal cord. The focally recorded presynaptic spike was not affected by the action of ether. The antidromic field potential of motoneurones, recorded from an extracellular position, was sensitive to the depressant action of ether.

Posttetanic potentiation was, at a similar level of fractional pool discharge, equal in magnitude in the unanesthetized state and at different levels of narcosis caused by thiopental or by ether. Input-output studies showed that the spatial summation required to secure any fractional pool discharge is increased by a similar amount by ether and by thiopental at an equivalent depth of narcosis. When Rall's (1955a) correction for "effective input" was applied, the input-output curves appeared to be shifted to the right with little change of slope.

It is concluded that the presynaptic terminals in the monosynaptic spinal reflex pathway conduct normal impulses at a depth of narcotic depression where the monosynaptic reflex is reduced to less than 10% of its control amplitude. The most probable explanation of the depression of synaptic potentials by anesthetic drugs is a nonspecific stabilization of the subsynaptic membrane; decrease of the amount of transmitter released per presynaptic impulse cannot be ruled out on the basis of available experimental data.