Abstract
The tricyclic antidepressant clomipramine (CIM) has been shown to inhibit the uptake of serotonin (5-hydroxytryptamine, 5-HT) into rat brain synaptosomes as well as into human platelets. The acute administration of CIM decreases 5-HT turnover (Carlsson and Lindqvist, 1978; Marco and Meek, 1979). This finding agrees with electrophysiological studies showing a reduction in the firing rate of 5-HT neurons after a single dose of CIM (Gallager and Aghajanian, 1975; Dresse and Scuvée-Moreau, 1979). The increased synaptic availability caused by the inhibition of 5-HT uptake possibly activates a feedback mechanism mediated by presynaptic and/or somatodendritic autoreceptors. This may lead to a decrease in the activity of 5-HT neurons thereby lowering its release.
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References
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© 1991 Plenum Press, New York
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Adell, A., Artigas, F. (1991). Effects of Clomipramine on Extracellular Serotonin in the Rat Frontal Cortex. In: Schwarcz, R., Young, S.N., Brown, R.R. (eds) Kynurenine and Serotonin Pathways. Advances in Experimental Medicine and Biology, vol 294. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5952-4_42
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DOI: https://doi.org/10.1007/978-1-4684-5952-4_42
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