Abstract
THAT d-tubocurarine (DTC) is convulsant when applied topically to the cerebral cortex has been known for many years but the mechanism of its action is still unclear1–3. Other neuromuscular blocking drugs such as gallamine, decamethonium and dihydro-β-erythroidine do not have this convulsive property4 and the usual comparison is with known convulsants such as picrotoxin and strychnine1,4,5. This suggests that different receptors to those in the periphery are involved in the convulsive action of DTC and it is possible that the central receptors with which DTC interacts may be those mediating cortical inhibitory processes. Blockade of these receptors would result in uncontrolled excitation and lead to paroxysmal discharges. As γ-aminobutyric acid (GABA) is now thought to be the cortical inhibitory transmitter6, we have examined the interactions of DTC and GABA, applying both substances by microiontophoresis. In addition we have studied the effects of microiontophoretically applied DTC on the inhibition of cortical neurones produced by direct shocks to the adjacent cortical surface7,8 and we have also compared DTC with other convulsants applied to the same neurones, from the same pipette.
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HILL, R., SIMMONDS, M. & STRAUGHAN, D. Convulsive Properties of d-Tubocurarine and Cortical Inhibition. Nature 240, 51–52 (1972). https://doi.org/10.1038/240051a0
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DOI: https://doi.org/10.1038/240051a0
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