[Carbonyl-C-11]WAY-100635 has been reported to be a useful ligand for the investigation of 5-HT1A receptor imaging in vivo. However, the cellular distribution and the influence of endogenous serotonin (5-HT) on in vivo binding have not been fully examined. In this study, we investigated the effect of 5,7-dihydroxytryptamine-produced destruction of 5-HT neurons, reserpine-induced 5-HT depletion, and fenfluramine-induced 5-HT increase on [carbonyl-C-11]WAY-100635 binding in vivo. There was no significant change in the uptake of [carbonyl-C-11]WAY-100635 in the slice of 5-HT denervated rat brain except in the raphe nucleus, where 5-HT cell bodies exist. There was no obvious effect of enhanced 5-HT release by fenfluramine or decreased release by reserpine on [carbonyl-C-11]WAY-100635 binding in the dissected brain region. No significant effect was observed in the time course of [carbonyl-C-11]WAY-100635 in the hippocampus and frontal cortex measured by PET. These results indicated that the in vivo binding of [carbonyl-C-11]WAY-100635 in the hippocampus and cerebral cortex mainly reflects postsynaptic 5-HT1A, receptor binding, and that this binding is not sensitive to endogenous 5-HT, Synapse 40:122-129, 2001, (C) 2001 Wiley-Liss, Inc.
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- DOI : 10.1002/syn.1033
- ISSN : 0887-4476
- Web of Science ID : WOS:000167552100004