Soman, an organophosphorus cholinesterase inhibitor, was used to produce cholinergic stimulation and convulsions in rats. Soman (1 or 2 × LD 50) elevated cyclic 3′5′ guanosine monophosphate (cGMP) levels in the cerebellum, before the onset of cholinergic symptoms, during the stage prior to convulsions, at doses which produced no convulsive activity (1/2LD 50) and greatly elevated cGMP levels at the onset and during convulsions. Pretreatment which reduced the convulsive activity of soman also attenuated the increase in cGMP in the cerebellum. The results indicated that soman-induced convulsions and the resulting increase in cerebellar cGMP concentrations could not be related solely to increased cholinergic activity or to muscarinic effects. Pretreatment of poisoned animals with antimusarinic or antinicotinic compounds or atropine plus an oxime (HI-6) which protected animals from the lethal effects of soman, had little effect on severity of convulsions or cGMP levels. On the other hand, both parameters were sensitive to anticonvulsants (i.e. clonazepam) which, are not thought to produce their effects via anticholinergic actions. In addition, intracerebroventricular injections of dibutyryl cGMP (dbcGMP) caused convulsions which were blocked by small doses of clonazepam but were only slightly affected by atropine or mecamylamine, given alone. Stimulation of climbing fibres to the cerebellum may result in the release of an excitatory amino acid which may subsequently cause elevation of cGMP. However, soman failed to alter cerebellar concentrations of putative excitatory or inhibitory neurotransmitters while destruction of these fibres with 3-acetylpyridine prior to injection of soman failed to block either the convulsions or the increase in cGMP concentrations. These results suggest that cGMP may play a role in the initiation and continuation of soman-induced convulsions which were not related to specific cholinergic receptors but to general neuronal excitation. The results also indicate the involvement of non-cholinergic mechanisms in soman-induced convulsions, and in the rise in cerebellar cGMP levels; however, the identity of these mechanisms was not known.