Figure 1.

In situ hybridization analysis of the effects of repeated administration of dopamine agonists on dopamine receptor and neuropeptide gene expression in the striatal complex of unilaterally 6-OHDA-lesioned rats. Coronal sections were hybridized with ³³P-labeled cRNA probes for D₁, D₂, or D₃ receptors (DRs), prodynorphin (DYN), or preproenkephalin (ENK) mRNAs, apposed to autoradiographic films and resulting pictures analyzed densitometrically. (a) Typical pictures showing the increased D₃ receptor mRNA in the lesion side (indicated by asterisk) of the dorsolateral striatum (CdPu), StPv, and shell or core subdivisions of nucleus accumbens (AcSh, AcCo) after a 5-day levodopa (l-DOPA) treatment and the blockade of this effect by SCH 23390 (SCH). The effect of levodopa was partially reproduced by SKF 38393 (SKF). ICj, islands of Calleja. (b) Mean D₃ receptor mRNA levels ± SEM (n = 4–6) in the two sides of CdPu (excluding StPv) and AcSh following repeated administration of vehicle or l-DOPA. (c) Mean percent difference (±SEM) in D₁, D₂, and D₃ receptor mRNA levels between lesion and control side of CdPu. Same animals as in b. The mean (±SEM) signals on the control side of vehicle-treated rats corresponded to 454 ± 54, 597 ± 63, and 8 ± 1 nCi/g (1 Ci = 37 GBq) for D₁R, D₂R, and D₃R, respectively. (d) Mean percent difference (± SEM, n = 4–6) in D₃R, DYN, and ENK mRNA levels between lesion and control side of CdPu following 5-day administration of levodopa alone or together with SCH of bromocriptine (BROMO), quinelorane (QUIN), or SKF. The mean (± SEM) in situ hybridization signal on the control side of vehicle-treated rats corresponded to 0.22 ± 0.03 and 1.7 ± 0.2 μCi/g for DYN and ENK, respectively. ∗, P < 0.05; ∗∗, P < 0.01 in lesion vs. control side by the paired Student’s t test; §, P < 0.05; §§, P < 0.01 in lesion side of drug vs. vehicle-treated animals by the Mann–Whitney U test.