DRUG EFFECTS ON THE SPONTANEOUS ELECTRICAL ACTIVITY OF THE SQUID GIANT AXON

¹ Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York

Squid giant axons exposed to sea water containing 25% of the usual concentration of Ca and Mg display spontaneous or repetitive electrical activity at rates up to 300/sec. The antiepileptic compounds, diphenylhydantoin, mephenytoin, trimethadione and phenobarbital, blocked this spontaneous activity in concentrations well below that which affected the evoked action potential, indicating considerable specificity in their action. Barbital and sodium bromide showed much less specificity. The antiparkinsonian compounds, trihexyphenidyl, caramiphen, benztropine and ethopropazine, also showed considerable specificity in blocking the hyperexcitable axon, whereas atropine showed no specificity. Trihexyphenidyl, benztropine and diphenylhydantoin had no effect on the resting potential. The following compounds showed less specificity in blocking the spontaneous firings than the antiepileptic or antiparkinsonian compounds: ether, chloroform, ethanol, procaine, tetracaine, chlorpheniramine and chlorpromazine. Pentylenetetrazol, strychnine, picrotoxin and oxotremorine had little or no effect on the spontaneously firing axon. Various other compounds were also ineffective in blocking this hyperexcitable axon. The spontaneously firing squid axon may serve as a convenient test system for the detection and analysis of action of antiepileptic and antiparkinsonian compounds.