Effect of chronic treatment with selective monoamine oxidase inhibitors and specific 5-hydroxytryptamine uptake inhibitors on [3h]paroxetine binding to cerebral cortical membranes of the rat

Changes in Human In vivo Serotonin and Dopamine Transporter Availabilities during Chronic Antidepressant Administration

“…This result suggests that the transporter density was unaltered in this limited but chronic period. Consistent with our results, several rodent studies found no change in SERT density after 14-21 days of citalopram treatment (Hyttel et al, 1984;Graham et al, 1987;Kovachich et al, 1992;Cheetham et al, 1993;Spurlock et al, 1994). By contrast, a recent careful study (Benmansour et al, 1999) showed 80-90% downregulation of rat hippocampal SERT density after chronic SSRI treatment of paroxetine or sertraline for 21 days.…”

Addition of Lithium to Chronic Antidepressant Treatment Potentiates Presynaptic Serotonergic Function without Changes in Serotonergic Receptors in the Rat Cerebral Cortex

“…There were no effects on the Kj and Bmax in any treatment. It is in agreement with a previous report that the Kj and Bmax of the binding of [3H]paroxetine to cerebral cortical membranes of the rat has been shown to be unaffected by the chronic adminis tration of CIT or CMI [16]. Judging from the above results, at least in the cerebral cortex, changes in 5-HT receptors may not be related to potentiation of the action of antidepressants by Li.…”

A Nonlinear Relationship between Cerebral Serotonin Transporter and 5-HT2AReceptor Binding: AnIn VivoMolecular Imaging Study in Humans

“…This interpretation is in accordance with our observation of a high interregional correlation of 5-HT 2A receptor binding, which is suggestive of a common regulator, presumably the raphe serotonergic output. Given that the 5-HT 2A receptor binding is accepted as a surrogate marker of cerebral 5-HT levels and that SERT binding adjusts to 5-HT levels in a manner suggested from some, although not all, experimental studies (Graham et al, 1987;Kovachich et al, 1992;Cheetham et al, 1993;Pineyro et al, 1994;Rattray et al, 1996;Gobbi et al, 1997;Benmansour et al, 1999;Horschitz et al, 2001;Benmansour et al, 2002;Evrard et al, 2002;Gould et al, 2003Gould et al, , 2006Rothman et al, 2003), our observation of an inverted U-shaped relation between 5-HT 2A receptor and SERT binding may be the result of inter-individual differences in cerebral baseline 5-HT levels.…”

“…In vitro autoradiography and homogenate binding experiments in rats suggest that a decrease in SERT binding levels occur after pharmacologically induced chronic extracellular 5-HT depletion in two (Rattray et al, 1996;Rothman et al, 2003) of three studies (no change seen in the study by Dewar et al, 1992). Chronically elevated extracellular 5-HT levels have usually been achieved by chronic treatment with the specific selective serotonin reuptake inhibitor (SSRI) compounds sertraline, citalopram, and paroxetine, and, in 10 ( Kovachich et al, 1992;Pineyro et al, 1994;Benmansour et al, 1999;Horschitz et al, 2001;Benmansour et al, 2002;Gould et al, 2003Gould et al, , 2006Rossi et al, 2008) of 15 experimental settings (no change reported in the studies by Graham et al, 1987;Kovachich et al, 1992;Cheetham et al, 1993;Gobbi et al, 1997;Gould et al, 2006), decreased SERT levels have been found. It can be argued, however, that chronic blockade of the SERT may lead to regulation of its expression and that the primary cause for the SERT downregulation is unrelated to 5-HT levels.…”