ACTION OF ETHER AND NEMBUTAL ON THE NERVOUS SYSTEM

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Abstract
The actions of ether and nembutal on the axon, the synapse, the rhythmically active nerve cell, the spinal cord, and the brain were analyzed in terms of the action potential changes they produce. The amplitude and the area of the axon spike potential and the negative after-potential are progressively diminished by ether and by nembutal. The electrical threshold of the axon is raised, its conduction rate is lessened, and its absolute refractory period is prolonged by ether and by nembutal. Ether markedly increases accommodation in the axon, nembutal decreases it slightly. Both ether and nembutal block conduction through a peripheral ganglion; they progressively lessen excitation of the soma through the synapse. Ether increases the frequency of discharge of nerve cells possessing spontaneous rhythmicity and nembutal decreases it, often without any initial increase. Both drugs first increase the magnitude of the response of nerve cells and then, with increasing anesthesia, decrease it. The increase produced by nembutal is considered to be in part a consequence of the reduction of the response frequency. Ether and nembutal differentially depress the immediate cortical response to saphenous nerve stimulation, the order of final extinction of its constituent waves being 3, 2, and 1. The general cortical excitation produced by spread is eliminated as the late waves are depressed. Excitation is an effect on the soma produced by the summation of brief electrical stimuli which arrive at the terminals of impinging nerve axons. A brief and a prolonged excitatory state develop in the soma following their action. Inhibition, aside from the well known rhythmical changes in responsiveness, results in a lowering or elimination of the potentials associated with activity and presumably would oppose the activation of nerve cells.

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