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  Vol. 26 No. 2, February 1972 TABLE OF CONTENTS
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Penicillin-Induced Segmental Myoclonus

II. Membrane Properties of Cat Spinal Motoneurons

Luke I. Kao, MD; Wayne E. Crill, MD

Arch Neurol. 1972;26(2):162-168.


Abstract

Penicillin was applied to the cat spinal cord and the changes in membrane properties of motoneurons measured. Just prior to the appearance of the facilitated spontaneous synaptic potentials, there is a diminution of the resting potential of the motoneuron. This is not associated with a detectable change in membrane resistance or in time constant. The after-hyperpolarization of the action potential is decreased. The simplest explanation for these changes is a change in the potassium equilibrium potential (Ek). To test the possibility that the change in Ek is causally related to the appearance of the prolonged depolarization, the intracellular potassium of normal motoneurons was displaced with either choline or tetramethylammonium ions. In both cases a prolonged depolarization occurred similar to that produced by penicillin, and, moreover, this response was evoked by directly applied intracellular currents.



Author Affiliations

Seattle

From the departments of medicine (Drs. Kao and Crill) and physiology and biophysics (Dr. Crill), Division of Neurology, University of Washington School of Medicine, Seattle.


Footnotes

Accepted for publication Aug 31, 1971.

Read in part before the annual meeting of the American Neurological Association, Washington, DC, June 15, 1971.

Reprint requests to Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98105 (Dr. Crill).



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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Dendritic mechanisms underlying penicillin-induced epileptiform activity
Wong and Prince
Science 1979;204:1228-1231.
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Penicillin-Induced Segmental Myoclonus: I. Motor Responses and Intracellular Recording From Motoneurons
Kao and Crill
Arch Neurol 1972;26:156-161.
ABSTRACT  

Penicillin-Induced Metabolic Alterations in Isolated Cerebral Cortex
Swanson
Arch Neurol 1972;26:169-174.
ABSTRACT  





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