Abstract
From the original insights of Jackson nearly a hundred years ago (1890) to the recent book by Lockard and Ward (1980), convulsive seizures have been viewed as a window into the functioning of the brain, the assumption being that pathophysiology yields considerable insight into normal physiology. Convulsant drugs have been a major tool over the years in trying to understand how and why the brain generates the extensive and dramatic electrical and behavioral events of generalized seizure. From Claude Bernard’s pioneering work on the effects of strychnine on the spinal cord to Jeff Barker’s investigations of convulsants in spinal cord neurons in culture (Barker et al., 1983), these chemical agents have been used as tools to aid in the understanding of the global events of epileptic disorders and as molecular probes of subsynaptic neuronal properties. Since the original discovery that physostigmine, the active ingredient in the calibar bean, was capable of prolonging the actions of a specific neurotransmitter, acetylcholine, the study of neurochemical actions of drugs with convulsant properties has developed into a dominant theme in investigations of the molecular bases of epilepsy. When Curtis and coworkers (1971) demonstrated that strychnine could specifically block the action of the inhibitory transmitter, glycine, which is a prominent neurotransmitter in the spinal cord (Werman et al., 1968; Young and Macdonald, 1983), this clearly represented an important mechanism subserving the ability of strychnine to produce the spinal seizures that Claude Bernard first observed so long before. Several useful reviews on convulsant drugs have been published previously (Hahn, 1960; Esplin and Zablocka-Esplin, 1969; Woodbury, 1980; Davidoff, 1983).
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Faingold, C.L. (1987). Seizures Induced by Convulsant Drugs. In: Jobe, P.C., Laird, H.E. (eds) Neurotransmitters and Epilepsy. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-462-7_9
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