1. Characterization of the Dopamine Defect in Primary Cultures of Dopaminergic Neurons from Hypoxanthine Phosphoribosyltransferase Knockout Mice 
Doug W. Smith, Theodore Friedmann 
Molecular Therapy 
Volume 1, Issue 5, Pages (May 2000)
DOI: /mthe
Copyright © 2000 American Society for Gene Therapy Terms and Conditions

2. FIG. 1
Photomicrographs showing DIV 15, dopamine neurons (TH-immunostained) from wild- type (A and B) and HPRT-deficient mesencephalic cultures (C and D), under control (A and C) and GDNF- supplemented conditions (B and D). Note the absence of obvious morphological differences between the dopamine neurons of the two genotypes and the similar survival and neurite outgrowth- promoting effects of GDNF.
Molecular Therapy 2000 1, DOI: ( /mthe )
Copyright © 2000 American Society for Gene Therapy Terms and Conditions

3. FIG. 2
Survival curves for dopamine neurons for wild-type and HPRT-deficient cultures under control and GDNF-supplemented conditions. Significant differences between control and GDNF-treated groups were apparent at days 5, 10, and 15 (in all cases P < ) but not at day 1. *** and ^^^ denote significant differences for wild-type and HPRT-deficient cultures, respectively. Thus, there was an interaction between treatment and DIV (F = 48.82, P < ) but not for genotype (F = 2.23, P < ) or any other interaction.
Molecular Therapy 2000 1, DOI: ( /mthe )
Copyright © 2000 American Society for Gene Therapy Terms and Conditions

4. FIG. 3
Dopamine uptake response at different time points for control and GDNF-supplemented wild-type and HPRT-deficient cultures. Statistical analysis revealed significant effects of genotype (F = 31.46, P < ), treatment (F = 41.12, P < ), and DIV (F = , P < ) and an interaction between treatment and DIV (F = 3.34, P < 0.05) but not between any other factors. # denotes significant (P < 0.05) difference in uptake between wild-type and HPRT-deficient GDNF-treated dopamine neurons. Uptake in control cultures was not significantly different between genotypes; dopamine uptake in wild-type cultures was significantly higher at DIV 5, 10, and 15 (F = 5.98, P < 0.05; F = 5.35, P < 0.05; F = 5.98, P < 0.05), but not at DIV 1 (F = 2.23, P < 0.16).
Molecular Therapy 2000 1, DOI: ( /mthe )
Copyright © 2000 American Society for Gene Therapy Terms and Conditions

5. FIG. 4
Dopamine content at DIV 5, 10, and 15 for control and GDNF-sup-plemented wild-type and HPRT-deficient dopamine neurons. Dopamine levels at DIV 1 were too low for reliable detection. Statistical analysis revealed significant main effects for genotype (F = 21.13, P < ), treatment (F = 123.3, P < ), and DIV (F = 35.3, P < ) but no interaction between any of these. Comparison of dopamine contents between wild-type and HPRT-deficient neurons at the three time points for GDNF and control conditions revealed significantly higher dopamine levels in wild-type GDNF-treated dopaminergic neurons compared to HPRT-deficient counterparts at DIV 5 and 10. The difference at DIV 15 did not reach statistical significance. There were no differences in dopamine content between genotypes under control conditions. # denotes significant (P < 0.05) difference between GDNF-treated wild- type and HPRT-deficient dopaminergic neurons.
Molecular Therapy 2000 1, DOI: ( /mthe )
Copyright © 2000 American Society for Gene Therapy Terms and Conditions