• 1 January 1978
    • journal article
    • research article
    • Vol. 207 (3), 825-836
Abstract
The site at which diethyl ether impairs transmission in the spinal monosynaptic pathway was studied by intracellular recording from lumbosacral motoneurons. The drug was administered by inhalation to spinal cats, in concentrations which produce surgical anesthesia. Ether had no significant effect on resting potential or input resistance of the cell membrane. It decreased the electrical excitability in some but not all motoneurons. This action may contribute to the depressant effects of ether. Monosynaptic excitatory postsynaptic potentials evoked by impulses in a single 1a afferent fiber (unitary EPSP) of the triceps surae nerve were recorded from homonymous motoneurons. They were measured and their amplitude distribution was analyzed by a computer-aided procedure. The mean amplitude of the unitary EPSP was 0.15-0.31 mV, and the mean number of transmitter quanta released by each impulse ranged from 1.5-4.1 before drug administration. Both values were decreased during inhalation of ether but recovered toward normal after the drug was discontinued. The mean amplitude of the EPSP produced by 1 transmitter quantum was 0.08-0.15 mV and was not depressed during ether administration. Ether in anesthetic concentrations depresses synaptic potentials presynaptically by decreasing the amount of excitatory transmitter released, while leaving the chemosensitivity of the postsynaptic membrane unchanged.