Objective: Harmaline and other beta-carbolines act as an inverse agonist for GABA-A receptors and cause central nervous system stimulation and anxiety; thus, it may act hypothetically as a potential seizure augmenter. To examine the hypothesis, the effect of harmaline during the seizures induced by amygdala kindling is investigated here. Methods: Seven groups of male rats were kindled by daily electrical stimulation of the amygdala. After being kindled, Groups I–III, respectively, received 5, 15 and 50 mg/kg harmaline through intraperitoneal injection. The rats in Groups IV and V received vehicle daily -1 ml/kg- and harmaline -5 mg/kg- daily through intraperitoneal injection. Groups VI and VII received artificial cerebrospinal fluid and harmaline -50 mM- through intraventricular injection, respectively. Results: In addition to significant increase of some seizure parameters in the fully kindled groups, harmaline significantly increased cumulative afterdischarge duration -P < 0.05- and decreased stage 1 latency -P < 0.01- in the acquisition groups -Groups V and VII-. In Group VII, seizure duration showed a significant increase -P < 0.01- while stage 1 latency and stage 4 latency decreased significantly -P < 0.01-. Discussion: According to the results, it is suggested that harmaline may increase neuronal activity and the production of high-frequency action potentials by stimulating NMDA receptors and inhibiting GABA receptors. Overall, drugs and plants containing harmaline may be harmful to epileptic-susceptible people during some traditionally and costume treatments, so these should be avoided.

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