Figure 3
Amphetamine facilitates D2R dimerization and the expression of high-affinity D2 receptors (D2high) in rat striatal brain slices. A-B, Western blot analysis of the expression levels of D2R dimers (A) and monomers (B) in rat striatal slices treated with or without AMPH (30 min, 10 μM). *Significantly different from control group (p < 0.05; n = 3). Data were analyzed by t-test. C, Bar graph summarizing the binding of [3H]domperidone in rat striatal slices treated with or without AMPH (30 min, 10 μM). ***Significantly different from control group (p < 0.001; n = 7 in control group and n = 6 in AMPH group). D, Graphs representing three samples out of six experiments. The competition between dopamine and [3H]domperidone showed a biphasic pattern. In control striata, low concentrations of dopamine (generally between 10 and 5,000 nM) inhibited the binding of [3H]domperidone by an average of 17 ± 1.4%. Higher concentrations of dopamine further reduced the binding of [3H]domperidone in a distinctly separate phase. There was a clear plateau between the high-affinity phase (i.e., at low concentrations of dopamine) and the low-affinity phase (i.e., at high concentrations of dopamine). The treatment with amphetamine increased the proportion of high-affinity D2 receptors to 38.8% ± 3.9%.