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. Author manuscript; available in PMC: 2022 Jan 28.
Published in final edited form as: Sci Transl Med. 2021 May 19;13(594):eaaw1564. doi: 10.1126/scitranslmed.aaw1564

Fig. 5. Loss of DAT function in DTDS can be restored both pharmacologically and using a gene therapy approach in the mDA model.

Fig. 5

(A) Uptake of tritiated DA at day 65 after neurons treated for 24 hour with pifithrin-μ (pif). Values are relative to protein concentration (n = 3, 4, 4, and 4 per line). (B) Measurement of tritiated DA uptake at day 65 in patient-derived mDA neurons transduced with either a lentivirus construct expressing GFP alone (LV GFP) or human SLC6A3 and GFP (LV hSLC6A3-GFP) (n = 3 for each). (C) Immunofluorescence analysis at day 65 for patient-derived dopaminergic neurons transduced with LV GFP or LV hSLC6A3-GFP. Cells are stained for TH/MAP2, and nuclei were counterstained with DAPI. Scale bar, 100 μm. (D) Quantification of MAP2-positive, TH-positive, and TH/MAP2− double-positive neurons at day 65 of differentiation in mDA neurons transduced with LV GFP or LV hSLC6A3-GFP (n = 3 for each). Both DTDS lines were independently compared to controls using two-tailed Student’s t test for all analyses.