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NEUROLOGY 1982;32:241
© 1982 American Academy of Neurology

Homotaurine (3 aminopropanesulfonic acid; 3APS) protects from the convulsant and cytotoxic effect of systemically administered kainic acid

Ruggero G. Fariello, Gregory T. Golden and Michele Pisa

Service of Neurology, VA Hospital, and Department of Medicine, Division of Neurology, The University of Texas Health Science Center at San Antonio, San Antonio, TX (Dr. Fariello), the Department of Anatomy, Medical University of South Carolina, Charleston, SC (Dr. Golden), and Kinsmen Laboratories, University of British Columbia, Vancouver, BC, Canada (Dr. Pisa).

Pretreatment of rats with homotaurine (3 aminopropanesulfonic acid; 3APS), a synthetic {gamma}-aminobutyric acid (GABA) analog, protected from the convulsant and cytotoxic action of systemically injected kainic acid (KA). Wet dog shaking (WDS) behavior was significantly reduced. Taurine, an inhibitory non-GABA-mimetic amino acid, and muscimol (another direct GABA-agonist) reduced the number of seizures and lesions in the brain but were less effective than homotaurine. Progabide (a GABA-agonist) did not modify kainic acid effects. The neurotoxicity of kainic acid could have been due to repetitive convulsive activity. Activation of GABA-mediated inhibition is an effective, but not the determinant means of preventing KA-induced abnormalities.

Address correspondence and reprint requests to Dr. Fariello, Department of Medicine, Division of Neurology, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78284.

This work was supported, in part, by the Epilepsy Foundation of America.

Parts of these studies have been presented to the American Academy of Neurology meetings in New Orleans, 1980 and Toronto, 1981.

Accepted for publication August 4, 1981.






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