Fig. 5.

Opioid receptor levels and G protein activation following striatal knockdown of CB₁R or D₂R or over-expression of CRIP1a. Data are shown as immunoreactive MOR1 and DOR1 protein levels as a percent of the contralateral control value (100%) (means ± SEM, n = 4 rats) in the striatum (checkered bar), globus pallidus (striped bar) and entopeduncular nucleus (solid bar), and analyzed by a paired Student’s two-tailed t-test (*p < 0.05, ^#p < 0.01, ^$p < 0.001. (a) Knockdown of CB₁R or D₂R, and over-expression of CRIP1a in the dorsal striatum did not significantly alter MOR1 protein levels in any regions measured. (b) Knockdown of CB₁R or D₂R and over-expression of CRIP1a significantly increased DOR1 protein levels as indicated. (c) Striatal brain slices were subjected to [³⁵S] GTPγS binding stimulated by the MOR1 agonist D-Ala2, NMe-Phe4, Gly-ol5]-enkephalin [10 μM] (checkered bar) or the DOR1 agonist [D-Pen2, D-Pen5]-enkephalin [10 μM] (solid bar). Data are reported as a percent of the contralateral control side (100%) (means ± SEM, n = 4 rats) from [³⁵S]GTPγS binding measured in triplicates), and were analyzed using a paired Student’s two-tailed t-test (*p < 0.05, ^$p < 0.001).