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In vitro autoradiograms of rat brain sections with [11C]TASP0410457 illustrated the abundant specific binding in the striatum and neocortex (Fig. 7a).
Visualization and quantification of dopamine transporter (DAT) binding in the striatum is an established diagnostic tool to detect nigrostriatal dopaminergic degeneration.
In vivo, pre-treatment with 1 mg/kg (2.9 μmol/kg) raclopride led to 17 39 % decrease in D2/3R-specific binding in the striatum.
This finding is in line with a previous PET study which reported a positive correlation between DAT and SERT binding in the striatum of PD patients [30].
Unfortunately, in the period in which the participants were recruited and imaged, selective SERT tracers for SPECT, like [123I]ADAM, were not available to assess SERT binding in the striatum [32].
Although it is not possible to measure SERT availability in the striatum using [123I]β-CIT, midbrain [123I]β-CIT binding is mainly associated with the binding to SERT, while binding in the striatum is mainly associated with binding to DAT [24].
Similar(43)
We obtained arterial blood samples for kinetic data analysis and found that the compound had a differential distribution in brain regions, with the highest binding potentials in the frontal and temporal cortices, intermediate binding potential in the thalamus, and low binding potentials in the striatum, hypothalamus, and brainstem.
Other SPECT and PET studies of dopamine transporter binding in ADHD have reported increased binding capacity in the striatum of adults and children with ADHD [ 21- 23, 47].
CSD also up-regulated NMDA, AMPA, kainate, GABA(A), serotonergic 5-HT(2), adrenergic alpha(2) and dopaminergic D1 receptor binding sites in the striatum [76].
Homologues with a shorter fluoroalkyl chain consistently showed greater D2/3R-specific-to-total binding ratios in the striatum than those with longer chains.
In contrast, TPH2 mRNA levels were significantly increased by 24% in the mid DR and by 12% in the caudal DR. MDMA treatment significantly decreased 125I-RTI-55 labeled SERT binding sites in the striatum, nucleus accumbens and cingulate cortex demonstrating a loss of 5-HT terminals.
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