Effects on dopamine neurotransmission
Sertraline is an inhibitor of dopamine uptake in vitro with an IC50 of 48 nm (Hyttel, 1993). No other SSRI shows a similar profile: Fluoxetine and paroxetine are the next most potent dopamine reuptake inhibitors with IC50’s of 5,000 and 5100 nm respectively. Tatsumi et al (1997) demonstrated more potent affinity in vitro of the human dopamine transporter for sertraline (KD = 25 ± 2nM) than nomifensine (KD = 56 ± 3nM). The in vivo effects of sertraline and fuoxetine on dopamine transmission have been compared in the nucleus accumbens of the rat (Sharp et al, 1999). Sertraline increased dopamine transmission via pre- (producing extracellular dopamine increases) and post – (producing increased D2 receptor function by increasing D2 receptor expression) synaptic mechanisms. In contrast fluoxetine increased dopamine transmission via post-synaptic mechanisms only.
A relevant consequence of the dopaminergic activity of sertraline may be seen in the effect of sertraline relative to other SSRIs on plasma prolactin levels. Serotonergic input increases the release of prolactin from the hypothalamus, and dopaminergic input has the opposite effect. Multiple dose paroxetine (Wing et al, 1996; Cowen & Sargent, 1997; Amsterdam et al; 1998), fluoxetine (Urban & Veldhuis, 1991), fluvoxamine (Price et al, 1989; Spigset & Mjöndal, 1997), and citalopram (Laine et al, 1997) have all been reported to generally increase prolactin levels. The increase in prolactin on these SSRIs may reflect lowered hypothalamic dopaminergic tone. In contrast to other SSRIs, however, sertraline does not appear to generally increase prolactin levels (Gordon et al, 1998). For example, in a 12-week study in 21 male patients with sexual paraphilias treated with 50-200mg/day of sertraline mean baseline plasma prolactin levels of 9.29 m g/l were reduced by 12%, 7%, 3% and 9% at weeks 4, 8, 12 and study endpoint, respectively (Bradford, 1995).
Dopaminergic activity may be the reason for the favorable effect of sertraline on DSST performance. In patients with Korsakoff’s amnesia, performance on the DSST and certain other measures of psychomotor function showed a positive correlation with the concentration of homovanillic acid, the major metabolite of dopamine, in the cerebrospinal fluid (McEntee et al, 1987) suggesting a dopaminergic basis for performance on these measures.
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