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Title: Decreased striatal and enhanced thalamic dopaminergic responsivity in detoxified cocaine abusers

Journal Article · · Journal of Nuclear Medicine
OSTI ID:563333
; ;  [1]
  1. Brookhaven National Lab., Stony Brook, NY (United States); and others

It has been hypothesized that cocaine addiction could result from decreased brain dopamine (DA) function. However, little is known about changes in (DA) neurotransmission in human cocaine addiction. We used PET and [C-11]raclopride, a DA D2 receptor ligand sensitive to competition with endogenous DA, to measure relative changes in extracellular DA induced by methylphenidate (MP) in 20 cocaine abusers (3-6 weeks after cocaine discontinuation) and 23 controls. MP did not affect the transport of [C-11]raclopride from blood to brain (K1); however it induced a significant reduction in DA D2 receptor availability (Bmax/Kd) in striatum. The magnitude of ND-induced changes in striatal [C-11]raclopride binding were significantly larger in controls (21 + 13% change from baseline) than in cocaine abusers (9 {+-} 13 %) (ANOVA p < 0.005). In cocaine abusers, but not in controls, MP also decreased Bmax/Kd values in thalamus (29 {+-} 35 %) (ANOVA p < 0.005). There were no differences in plasma MP concentration between the groups. In striatum MP-induced changes in Bmax/Kd were significantly correlated with MP-induced changes in self reports of restlessness (r = 0.49, df 42, p < 0.002). In thalamus MP-induced changes in Bmax/Kd were significantly correlated with ND-induced changes in self reports of cocaine craving (r = 0.57, df 42, p < 0.0001). These results are compatible with a decrease in striatal DA brain function in cocaine abusers. They also suggest a participation of thalamic DA pathways in cocaine addiction.

OSTI ID:
563333
Report Number(s):
CONF-970602-; ISSN 0161-5505; TRN: 97:004028-0005
Journal Information:
Journal of Nuclear Medicine, Vol. 38, Issue Suppl.5; Conference: 44. annual meeting of the Society of Nuclear Medicine, San Antonio, TX (United States), 2-5 Jun 1997; Other Information: PBD: May 1997
Country of Publication:
United States
Language:
English