Starting from the idea that different primary actions of carbamazepine, valproate and lithium might converge into a similar secondary mechanism of action, e.g. a modulation of the functioning of certain transmitter systems, a review of the literature was made on the effects of these and related substances on GABAergic, dopaminergic, cholinergic, noradrenergic and serotonergic transmission, in an attempt to find a common denominator. It was concluded that similarities of the effects of these drugs are most evident with respect to a reduction of dopaminergic transmission. Some similarities also exist with respect to GABAergic and, to a lesser degree, cholinergic transmission. The effects on noradrenergic and serotonergic transmission seem too disparate to be considered as a potential basis for the antimanic effects of these drugs.

Abstract. N,N-dimethyltryptamine (DMT) is a psychotomimetic indolealkylamine that has been suspected of being an endogenous causal factor in the aetiotogy of schizophrenia. Some aspects of its interaction with the dopaminergic system of the rat brain have been studied neurochemically, and comparisons have been made with the effects of d-amphetamine and apomorphine. In contrast to these two compounds, DMT has proved to be a potent, but short-acting MAO inhibitor with a rather selective effect on MAO A (serotonin-deaminating MAO).Like classical MAO inhibitors, DMT also greatly increases the accumulation of 3 H-dopamine plus 3 H-3-methoxytyramine newly formed from 3H-Dopa. Amphetamine and apomorphine have no comparable effect.Striatal levels of 3,4-dihydroxyphenylacetic acid are more efficiently lowered by DMT than those of homovanillic acid. The reverse has been observed with apomorphine, whereas amphetamine increases the concentrations of homovanillic acid and decreases those of 3,4-dihydroxyphenylacetic acid.Thus, in addition to its MAO inhibitory action, DMT probably also possesses dopamine-releasing effects. Both these properties could result in an indirect dopaminomimetic activity of DMT. It may be assumed, therefore, that the psychotomimetic activity of this compound is not only linked to its effects on cerebral serotonergic mechanisms, but to a combination of these with an indirect dopaminergic stimulant activity.

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Combined treatment with amfonelic acid and neuroleptics caused a considerable loss of striatal, but not cortical 5-hydroxytryptamine (5-HT) in rats. This could be prevented by pretreatment with the specific 5-HT uptake inhibitor, citalopram. The results are best explained by the assumption that the combined treatment with amfonelic acid and neuroleptic had massively released dopamine into the synaptic cleft, and a part of this had been taken up into the 5-HT neurons by the 5-HT uptake mechanism and displaced the indoleamine.