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Striatal binding of the PET ligand 11 C‐raclopride is altered by drugs that modify synaptic dopamine levels
Author(s) -
Dewey Stephen L.,
Smith Gwenn S.,
Logan Jean,
Brodie Jonathan D.,
Fowler Joanna S.,
Wolf Alfred P.
Publication year - 1993
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890130407
Subject(s) - raclopride , tetrabenazine , dopamine , binding potential , chemistry , striatum , amphetamine , pharmacology , dopaminergic , dopamine receptor d2 , neuroscience , medicine , psychology
Bilatera decreases in striatal 11 C‐raclopride binding were observed in adult female baboons with high resolution PET following administration of drugs that act centrally on dopaminergic neurons. At baseline and following administration of d‐amphetamine (a dopamine‐releasing drug), GBR‐12909 (a potent dopamine reuptake inhibitor), or tetrabenazine (a biogenic amine depleting drug) PET scans of 11 C‐raclopride binding were obtained in a CTI 931 positron tomograph. In all studies, the ratio of the distribution volumes for the striatum to the cerebellum for 11 C‐raclopride binding decreased significantly by an average of 16.2% for d‐amphetamine, 22.1% for GBR‐12909, and 28.3% for tetrabenazine while there were no significant changes observed in the cerebellum or in the rate of systemic metabolism of the radiotracer. These decreases exceed the test/retest variability of striatal 11 C‐raclopride binding measured in the same animals under identical experimental conditions (Dewey et al., 1992b). Together these studies demonstrate that PET measurements of striatal 11 C‐raclopride binding can be used to indirectly and non‐invasively monitor changes in synaptic dopamine concentrations that result from a variety of neurophysiologic mechanisms. © 1993 Wiley‐Liss, Inc.