@article {Bosker:March 2001:0022-3042:1645,
author = "Bosker, F. J.",
author = "Cremers, T. I. F. H.",
author = "Jongsma, M. E.",
author = "Westerink, B. H. C.",
author = "Wikstrom, H. V.",
author = "den Boer, J. A.",
title = "Acute and chronic effects of citalopram on postsynaptic 5-hydroxytryptamine1A receptor-mediated feedback: a microdialysis study in the amygdala",
journal = "Journal of Neurochemistry",
volume = "76",
year = "March 2001",
abstract = "Microdialysis was used to assess the involvement of postsynaptic 5-hydroxytryptamine1A (5-HT1A) receptors in the regulation of extracellular 5-HT in the amygdala. Local infusion of the 5-HT1A receptor agonist flesinoxan (0.3, 1, 3 µm) for 30 min into the amygdala maximally decreased 5-HT to 50% of basal level. Systemic administration of citalopram (10 µmol/kg) increased 5-HT to 175% of basal level. Local infusion of 1 µmof the 5-HT1A receptor antagonist WAY 100.635 into the amygdala augmented the effect of citalopram to more than 500% of basal 5-HT level. 5-HT1A receptor responsiveness after chronic citalopram treatment was determined in two ways. First, by local infusion of 1 µmflesinoxan for 30 min into the amygdala, which showed a significant 63% reduction in response (area under the concentration-time curve; AUC) for the citalopram group compared to the saline group. Second, by systemic administration of citalopram (10 µmol/kg), which increased 5-HT to 350% of basal level. The effect was larger than in untreated animals, but more important, local infusion of 1 µmWAY 100.635 into the amygdala now failed to augment the effect of citalopram. Both the flesinoxan and WAY 100.635 data suggest an involvement of postsynaptic 5-HT1A receptor-mediated feedback in the amygdala, which diminishes following chronic citalopram treatment.",
pages = "1645-1653(9)",
url = "http://www.ingentaconnect.com/content/bsc/jnc/2001/00000076/00000006/art00007"
doi = "doi:10.1046/j.1471-4159.2001.00194.x"
}