Abstract
The anticonvulsant activity of baclofen, a putative γ-aminobutyric acid agonist, was determined in four different models of experimentally induced convulsions. These convulsions were induced by (i) transcorneally administered electroconvulsive shock, (ii) pentylenetetrazol administration, (iii) ringing sound presented to animals during barbital abstinence syndrome, and (iv) administration of 3-mercaptopropionic acid. The results showed the drug to be active as an anticonvulsant whether convulsions were induced by electroshock, 3-mercaptopropionic acid, or auditory stimulation. No effect was seen on convulsions induced by pentylenetetrazol administration. The participation of mechanisms involving the neurotransmitter γ-aminobutyric acid is suggested, and possible mechanisms of baclofen action are discussed.
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