The Influence of Cannabidiol and Δ9‐Tetrahydrocannabinol on Cobalt Epilepsy in Rats

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Abstract
The mechanisms of the anticonvulsant activity of cannabidiol (CBD) and the central excitation of .DELTA.9-tetrahydrocannabionl (.DELTA.9-THC) were studied electrophysiologically with conscious, unrestrained cobalt epileptic rats. The antiepileptics trimethadione (TMO), ethosuximide (ESM) and phenytoin (PHT) were included as reference drugs. Direct measurements were made of spontaneously firing, epileptic potentials from a primary focus on the parietal cortex and convulsions were monitored visually. ESM and TMO decreased the frequency of focal potentials but PHT and CBD exerted no such effect. CBD did not suppress the focal abnormality but did abolish jaw and limb clonus; .DELTA.9-THC markedly increased the frequency of focal potentials, evoked generalized bursts of polyspikes and produced frank convulsions. 11-OH-.DELTA.9-THC, the major metabolite of .DELTA.9-THC, displayed only 1 of the excitatory properties of the parent compound, production of bursts of polyspikes. .DELTA.9-THC and its 11-OH metabolite, CBD, even in very high doses did not induced any excitatory effects of convulsions. Apparently CBD exerts anticonvulsant activity against the motor manifestations of a focal epilepsy and that the mechanism of the effect may involve a depression of seizure generation or spread in the CNS.