Abstract

The effect of chronic citalopram or escitalopram administration on 5-HT 1A receptor function in the dorsal raphe nucleus was determined by measuring [ 35S]GTPγS binding stimulated by the 5-HT 1A receptor agonist ( R)-(+)-8-OH-DPAT (1nM–10 μM). Although chronic administration of citalopram or escitalopram has been shown to desensitize somatodendritic 5-HT 1A autoreceptors, we found that escitalopram treatment decreased the efficacy of 5-HT 1A receptors to activate G proteins, whereas citalopram treatment did not. The binding of [ 3H]8-OH-DPAT to the coupled, high affinity agonist state of the receptor was not altered by either treatment. Interestingly, escitalopram administration resulted in greater occupancy of serotonin transporter sites as measured by the inhibition of [ 3H]cyanoimipramine binding. As the binding and action of escitalopram is limited by the inactive enantiomer R-citalopram present in racemic citalopram, we propose that the regulation of 5-HT 1A receptor function in the dorsal raphe nucleus at the level of receptor-G protein interaction may be a result of greater inhibition of the serotonin transporter by escitalopram.

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