The mechanisms for the excitability changes produced by ether on the electrical activity of frog skeletal muscle were investigated by intracellular microelectrode techniques. Low concentrations of ether (less than 1%) increased excitability by increasing the 'effective resistance' between the inside and the outside of the fiber at the point of stimulation, thereby reducing the current needed to initiate an action potential. Higher concentrations decreased excitability by inhibiting the specific increase in sodium conductance which normally follows an adequate stimulus and is responsible for the rising phase of the action potential.

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KAMIYAMA, A., and INOUE, F. 1971. Conduction delay from Purkinje fiber to ventricular muscle studied with extracellular microelectrodes. Can. J. Physiol. Pharmacol. 49, 678-684.The relationship between electrical activity recorded intracellularly and extracellularly was studied in canine right ventricle. When the tip of a microelectrode was placed against a Purkinje fiber the electrical activity obtained had two components. The first component was a sharp diphasic wave which was defined as an action current while the second component was a rounded and flat diphasic wave which was defined as a field potential. Transmembrane action potentials recorded at the same site indicated that the first component was an active membrane current of the Purkinje fiber while the second component was identified as the field effect potential generated by ventricular fibers lying directly under the layer of Purkinje fibers. In areas where the Purkinje fibers were absent only the second component was present. The time delay of approximately 5 ms between the two components represents the conduction delay of the impulse from the Purkinje fiber to the ventricular fiber. KAMIYAMA,A,, et INOUE, F. 1971. Conduction delay from Purkinje fiber to ventricular muscle studied with extracellular microelectrodes. Can. I. Physiol. Pharmacol. 49, 678-684. Sur des fragments de tissus ventriculaire droit, nous avons ttudit les relations entre I'activitC tlectrique intra et extracellulaire. Lorsque la pointe de la microtlectrode est positionnte au dessus d'une cellule de Purkinje, I'activitk tlectrique enregistrte prtsente deux composantes. La premihre, dCfinie comme un courant d'action, est constitute d'une onde rapide et diphasique.La seconde consiste en une onde diphasique lente et rtsulte d'un champ de potentiel. Par comparaison avec I'activitt Clectrique intracellulaire, il apparai"t que la premihre composante rtsulte d'un courant membranaire des cellules de Purkinje tandis que la second risulte d'un champ de potentiel crtC par les fibres ventriculaires sous-jacentes. Au niveau des regions dtpourvues de cellules de Purkinje, seule la seconde composante est enregistrte. La latence entre les deux composantes est de l'ordre de 5m sec reprtsentant le temps de conduction de I'influx entre les cellules de Purkinje et les cellules ventriculaires.

No abstract

By recording simultaneously from muscle fibers and from the ventral root supplying the muscle, it was found that low concentrations of tetraethylammonium (TEA) caused the muscle fibers to fire without antidromic impulses being conducted to the ventral root. Exposing the muscles to higher TEA concentrations induced action potential firing in both the muscle and the ventral root. d-Tubocurarine prevented the muscle fiber activity but did not modify the ventral root firing. The application of a single supramaximal electrical stimulus to the sciatic nerve resulted in an afterdischarge of the muscle fibers either alone or simultaneous with an afterdischarge of fibers in the ventral root. By recording from fine intramuscular motor nerve fibers with extracellular glass capillary microelectrodes while simultaneously recording from the ventral root, it was demonstrated that TEA could cause these fine intramuscular motor nerve fibers to fire without the activity being conducted antidromically to the ventral root. A consideration of the patterns of TEA-induced electrical activity and afterdischarging led to the suggestion that TEA causes these effects by displacing calcium from binding sites on the motor nerve endings, making the latter hyperexcitable and unstable and thereby causing afterdischarging and 'spontaneous' activity.