Striatal presynaptic monoaminergic vesicles are not increased in Tourette's syndrome

Background: Abnormal function of striatal dopaminergic synapses is suggeste d to underlie Tourett's syndrome (TS). Objective: To determine dorsal stria tal dopaminergic innervation in TS. Prior in vitro and in vivo studies of d opamine reuptake transporter binding sites suggest increased striatal dopam inergic innervation in TS. Methods: We used in vivo measures of striatal ve sicular monoamine transporter type-2 (VMAT2) binding to quantify striatal d opaminergic innervation in TS. Eight TS patients (mean age 30 +/- 9 years) and 22 age-comparable normal controls (age 34 +/- 8 years) underwent PET im aging with the VMAT2 ligand (+)-alpha-[C-11]dihydrotetrabenazine (DTBZ). Co mpartmental modeling was used to quantify blood-to-brain ligand transport a nd VMAT2 binding site density from the tissue-to-plasma distribution volume (DV) during continuous (+)-alpha-[C-11]DTBZ infusion. DTBZ DV in dorsal st riatal regions was expressed relative to the occipital cortex to estimate r elative specific VMAT2 binding (binding potential). Results: We found no si gnificant differences in VMAT2 binding potential between patients and contr ols in the caudate nucleus, anterior putamen, or posterior putamen. There w ere no significant differences in striatal VMAT2 binding between patients w ith (n = 5) or without (n = 3) features of obsessive-compulsive disorder. C onclusions: There is no evidence for increased binding to the VMAT2 in TS s triatum and that dorsal striatal dopaminergic innervation density is normal in TS. The previously reported changes in dopamine transporter binding sit es may reflect medication effect and/or altered synaptic activity or regula tion of dopamine transporter expression in nigrostriatal neurons.