Abstract
The mechanism by which diethyl ether and thiopental interrupt the transmission of the monosynaptic reflex in the mammalian spinal cord has been studied by recording ventral root potentials and by microelectrode studies of single motoneurones. On ventral root records the voltage at which the propagated spike appears to depart from the synaptic potential was reversibly increased by the administration of the drugs. The rate of rise of the synaptic potential was reduced. Intracellular records revealed a reversible increase of the depolarization required to initiate an orthodromic impulse (and an elevation of the trigger level of transmembrane potential), in 15 out of 31 motoneurones. The resting membrane potential was not changed in a consistent or significant way. The synaptic potential (EPSP) was shown to be depressed by anesthetics in all cases where its amplitude could be measured (27 cells).
No delay of the onset of the synaptic potential could be detected by either the extra-, or the intracellular method of recording at the applied dosages of the anesthetics.
In 25 out of 33 motoneurones the configuration of the antidromic spike was unaltered in spite of profound depression of synaptic function by ether. In 8 cells antidromic invasion was reversibly blocked by a reduction of the amplitude of the initial small (A or IS) spike.
The mechanisms of action of ether and thiopental could not be distinguished from each other by the methods employed in this study.
Footnotes
- Received October 12, 1962.
- Accepted January 28, 1963.
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