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. 2023 Jan 19;14:1002960. doi: 10.3389/fnsyn.2022.1002960

FIGURE 2.

FIGURE 2

(I) Expression of SP and D1 in striatonigral and ENK and D2r in striatopallidal neurons. Striatal neurons retrogradely labeled with the fluorescent dye fluorogold after injection into the substantia nigra combined with darkfield illumination of silver grains produced by ISHH labeling with 35S labeled oligonucleotide probes for (A) substance P (SP), (B) the DI dopamine receptor (DI), (C) enkephalin (ENK), and (D) the D2 dopamine receptor (D2). Striatonigral neurons show ISHH labeling for both substance P [(A), solid arrows] and the D1 dopamine receptor [(B), solid arrows]. Striatal neurons that are unlabeled by fluorogold, and presumably project to the globus pallidus, show ISHH labeling for both enkephalin [(C), open arrows] and the D2 dopamine receptor [(D), open arrows]. (II) In situ hybridization in the striatum from brain sections apposed to autoradiographic film labeled with 35S-labeled oligonucleotide probes complementary to (A–D) enkephalin (ENK), (E–H) substance P (SP), and (I–L) dynorphin (DYN). Sections in the first two columns are from the same saline-treated animal showing ISHH labeling on the unlesioned control side (A,E,I) and lesioned 6-OHDA-injected side (B,F,J). Sections in the third column are from the lesioned, 6-OHDA-injected side of an animal that received intermittent treatment with the D1 receptor selective agonist SKF38393 (C,G,K). Sections in the fourth column are from the lesioned, 6-OHDA-injected lesioned side of animal that received continuous treatment with the D2 agonist quinpirole (D,H,L). The increase in enkephalin ISHH labeling caused by 6-OHDA lesions (B) is not affected by D1 agonist treatment (C) but is reversed by continuous D2 agonist treatment (D). The decrease in substance P ISHH labeling caused by 6-OHDA lesions (F) is reversed by intermittent D1 agonist treatment (G) but is unaffected by D2 agonist treatment (H). Dynorphin ISHH labeling is not significantly altered by 6-OHDA lesions (J) but is elevated by D1 agonist treatment (K) but not affected by D2 agonist treatment (L) (Gerfen et al., 1990).