Abstract
A central action of gallamine tniethiodide has been demonstrated in cats with implanted electrodes that permitted direct repetitive stimulation and recording of afterdischarges from cerebral cortex. Intravenously administered gallamine, at doses just sufficient to produce skeletal muscle paralysis, produced a consistent and reproducible augmentation of the duration of cortical afterdischarge. Simultaneous examination of expiratory carbon dioxide levels, blood pressure, body temperature and blood glucose in these animals did not reveal any consistent peripheral change to which the centrally observed effect could be attributed. Surgical transection of the spinal cord at C1 failed to block the gallamine-induced increase in afterdischange duration. Experiments on isolated cortical slabs also demonstrated an increase in afterdischarge duration after systemic gallamine. d-Tubocuranine, succinylcholine, decamethonium and dihydro-β-erythroidine consistently failed to produce increases in duration of afterdischarge under the same conditions.
Footnotes
- Received October 16, 1967.
- Accepted March 7, 1968.
- © 1968, by The Williams & Wilkins Company
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