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Zimelidine (ZIM) and its main active metabolite norzimelidine (NZIM) have been shown to preferentially inhibit 5-hydroxytryptamine (5-HT) neuronal uptake both in vitro and in vivo while having much less effect on noradrenaline (NA) uptake. ZIM in vivo blocked the 5-HT uptake mechanism in the cerebral cortex, hippocampus, striatum, hypothalamus and spinal cord, thus indicating effects on both the ascending and descending 5-HT pathways. ZIM is devoid of a 5-HT releasing action, MAO-inhibitory properties and effects on dopamine (DA) uptake. ZIM failed to reduce NA turnover even in high doses, but markedly reduced 5-HT turnover in very low doses in the rat. ZIM also enhanced 5-HT mediated behaviours in mice in doses related to the inhibition of 5-HT uptake. In contrast to amitriptyline (AMI) and mianserin (MIAN), ZIM only in extremely high doses displayed a 5-HT receptor blocking action in vitro and failed to block 5-HT mediated behaviour. ZIM was practically devoid of action on histamine H1 and H2 receptors, and had also a neglible action on noradrenergic alpha 1- and alpha 2-receptors, and on beta-receptors. Unlike the tricyclic antidepressants (TAD's) ZIM had a negligible action on muscarinic receptors and failed to affect cholinergic induced activity. Long-term treatment with ZIM did not result in any attenuation of the 5-HT uptake blocking potency or the reduction of 5-HT turnover. This long-term treatment slightly reduced the number of beta-receptors in the brain. However, repeated ZIM-treatment induced a new 5-HT receptor binding site characterized by a low affinity and with a high number of binding sites and decreased the number of high affinity 5-HT receptor binding sites. Unlike the TAD's zimelidine failed to block the action of reserpine. Metabolic and behavioural interactions studies in mice showed that ZIM was devoid of any significant interactions with ethanol, barbiturates and benzodiazepines. It is concluded that ZIM markedly differs from both the TAD's and new antidepressants such as mianserin and nomifensine. ZIM seems preferentially to effect the presynaptic 5-HT reuptake mechanism while having a negligible action on noradrenergic, 5-HT, acetylcholine and histamine receptors in the brain.
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