On some relationships between gamma-aminobutyric acid (GABA) and the cholinergic mechanisms in pentylenetetrazol convulsions.

In experiments on albino mice with pentylenetetrazol convulsions it has been found that GABA, introduced intracerebroventricularly in a dose of 100 microgram/mouse, has a marked anticonvulsive effect. Scopolamine in doses of 1, 10 and 50 mg/kg i. p. does not influence significantly the convulsive-seizure reactions, while spasmolytin inhibits them only in large doses (80 mg/kg weight). The inhibitory effect of GABA does not change significantly on the background of scopolamine, while spasmolytin in a dose of 50 mg/kg (and to a lesser extent 80 mg/kg) antagonizes the inhibitory effect of GABA. Arecoline in doses of 1 and 10 mg/kg inhibits to a certain extent the convulsive-seizure reactions, and in doses of 10 mg/kg it potentiates the effect of GABA. Physostigmine in doses of 0.1 and 0.5 mg/kg has no significant effect, while in a dose of 0.3 mg/kg its effect is inhibitory. On the background of the two higher physostigmine doses, however, the anticonvulsive effect of GABA is markedly decreased. The results show that changes in the functional activity level of the brain cholinergic systems lead to changes in the inhibitory effect of GABA on the convulsive reactivity. The mechanisms of these correlations are complex. However, the results are in support of the view that the balance between the different neurotransmitter systems in the brain and not a separate specifically responsible neurotransmitter system, are of decisive significance for the convulsive excitability and reactivity.