Taken together, the immunohistochemical measurements on DAT density correlate well with the electrochemistry data on DA clearance and suggests that the decreased DA clearance in Nurr1 mice after 2XMETH could be due to an elevated loss of DAT protein in the neuronal terminals.
Measurements of DAT revealed more widespread dopaminergic deficits compared to DA.
On the other hand, in vivo measurement of dopamine in DAT homozygous knockout mice shows a significant reduction in dopamine release triggered by burst stimulation [38] [40].
As expected, a high degree of positive correlation was found between the striatal DAT binding of [123I]β-CIT and measurements of TH- and DAT-reactive fiber densities in the rat striatum (Pearson correlation, P < 0.0001 at both time points) (Figure 3).
To investigate the binding property of Dat for its substrate and cofactor, ITC measurements were used to accurately determine the binding parameter and thermodynamic characterizations of Dat with dopamine and AcCoA respectively.
No clear progression of the lesion could be seen in either TH-reactive cell counts or TH- or DAT-reactive fiber density measurements.
As shown in Fig. 1, the average root diameter estimated by measurement of maximal root diameter at 10, 15, 20, 30 DAT were 0.96 mm, 2.12 mm, 3.36 mm, and 6.85 mm, respectively.
Measurements of d were taken in the Achilles tendon (dAT) and patellar tendon (dPT) using magnetic resonance imaging.
After 3 baseline measurements, rats were injected with MSI-1436 (10 mg/kg), the known DAT blocker bupropion (80 mg/kg) or saline and evoked DA release and reuptake were monitored for an additional hour.
Solvent accessibility measurements also revealed subtle differences in inhibitor positioning within a given DAT conformation.
