Abstract
In the published article, there was an error in the legend for Figure 2 as published. The corrected legend for Figure 2 appears below. “Figure 2. Establishment of motor deficits and development of Levodopa-induced dyskinesia (LID) in a bilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease. (A) The forepaw adjusting steps (FAS) test was employed 3 weeks after surgery to examine baseline motor impairments in bilateral 6-OHDA (n = 16; 8 M, 8 F) or sham (n = 16; 9 M, 7 F) -lesioned animals. FAS data are expressed as mean total steps + standard error of the mean (SEM). Baseline FAS data were analyzed with an independent-samples t-test (sham vs. lesion, *p < 0.05 vs. sham). (B) A subset of rats (n = 8; 4 M, 4 F) were administered daily LD (6 mg/kg; s.c) for 28 days and tested for the abnormal involuntary movements (AIMs) on days 1, 7, and 14. All rats were rated for axial, limb, and orolingual (ALO) behaviors for 3 h post-injection during AIMs sessions. ALO AIMs sums are expressed as medians + median absolute deviation (MAD). Significant within-subjects AIMs differences between lesion animals were found with a non-parametric Friedman ANOVA with Wilcoxon Match pairs post-hoc tests (*p < 0.05 day 1 vs. day 7; day 1 vs. day 14). Individual data points represented as • males, Δ females.” In the published article, there was an error in the legend for Figure 3 as published. The corrected legend for Figure 3 appears below. “Figure 3. The effects of bilateral 6-hydroxydopamine (6-OHDA) lesion and history of levodopa (LD) treatment on prepulse inhibition (PPI). In a between-subjects counterbalanced design, rats were treated with daily LD Vehicle (VEH) or LD (6 mg/kg; s.c.) for 4 weeks. (A) To examine PPI effects as a result of chronic treatment history, a 4 (Chronic treatment: sham VEH, sham LD, lesion VEH, lesion LD) × 3 (Prepulse condition: 70, 75, 80) mixed ANOVA was used for analyses (*p < 0.05, main effect of prepulse; *p < 0.05, main effect of chronic treatment). (B) To test lesion and LD's chronic effects compared to controls, PPI data from acute Compound 21 Vehicle (C21 VEH) days were analyzed with a 2 (Group: sham VEH vs. lesion LD) × 3 (Prepulse condition: 70, 75, 80 dB) mixed ANOVA with least significant difference (LSD) pairwise comparisons (*p < 0.05, prepulse 70 and 75). PPI data are presented as mean percent PPI values + standard error of the mean (SEM). Individual data points represented as • males, Δ females.” In the published article, there was an error in the legend for Figure 4 as published. The corrected legend for Figure 4 appears below. “Figure 4. Effects of acute compound 21 (C21) on levodopa-induced dyskinesia (LID), and motor performance in levodopa (LD)-treated animals. In a within-subjects counterbalanced design rats were treated acutely with C21 Vehicle (VEH) + LD, C21 (3 mg/kg; i.p.) + LD (6 mg/kg; s.c.), and C21 (6 mg/kg; i.p.) + LD (6 mg/kg; s.c.). (A) Abnormal involuntary movements (AIMs) were assessed for 3 h post LD-injection on all testing days. Axial, limb, and orolingual (ALO) AIMs are expressed as medians (ALO + median absolute deviation; MAD; n = 8; 4 M, 4 F). Total ALO AIMS were analyzed with non-parametric Friedman ANOVAs with Wilcoxon Match Pairs post-hocs (*p < 0.05 vs. VEH-LD). (B) Animals performed the forepaw adjusting steps (FAS) test 60 min post-LD administration on the same days that the AIMs test was performed (n = 8/group). FAS data are expressed as mean adjusting steps + standard error of the mean (SEM). FAS data were analyzed with a 2 [Lesion condition: lesion (n = 8) or sham (n = 8)] × 4 [Acute treatment: baseline, C21 VEH + LD, C21(3) + LD, C21(6) + LD] mixed ANOVA with least significant difference (LSD) post-hocs when appropriate (p < 0.05 lesion × treatment interaction). Individual data points represented as • males, Δ females.” In the published article, there was an error in the legend for Figure 5 as published. The corrected legend for Figure 5 appears below. “Figure 5. The effects of acute compound 21 (C21) treatment on prepulse inhibition (PPI). In a within-subjects counterbalanced design rats were treated acutely with Compound 21 (C21) Vehicle (VEH) + Levodopa (LD; 6mg/kg), C21 (3mg/kg) + LD (6 mg/kg), C21 (6 mg/kg) + LD (6 mg/kg). Rats were tested on PPI 45 min post-acute drug treatment while using their previous chronic treatment groups (sham VEH, sham LD, lesion VEH, lesion LD) as a grouping variable. A 4 (Chronic treatment: sham VEH, sham LD, lesion VEH, lesion LD) × 3 [acute treatment: C21 VEH, C21(3mg/kg), C21(6mg/kg)] mixed ANOVA was run and revealed a significant effect of chronic treatment group (*p < 0.05). Least significant difference (LSD) post-hocs suggested lesion LD animals showed significantly impaired PPI at all doses on C21 compared to all other chronic groups (*p < 0.05). PPI data are presented as mean percent PPI values + standard error of the mean (SEM). Individual data points represented as • males, Δ females.” In the published article, there was an error in the legend for Figure 6 as published. The corrected legend for Figure 6 appears below. “Figure 6. Loss of tyrosine hydroxylase (TH) immunoreactive neurons following bilateral 6-hydroxydopamine (6-ODHA) lesion and chronic treatment. (A) Representative images of TH immunoreactivity of nigral sections from each experimental group with circles indicating where cells were counted for each slice. (B) Total TH neuron loss quantified in the substantia nigra (SN) between sham and lesion rats either treated chronically with levodopa (LD) or vehicle (VEH; *p < 0.05 lesion condition; *p < 0.05 chronic treatment). (C) Total TH neuron loss quantified in the SN between all sham and lesion groups collapsed across chronic treatments (*p < 0.05 vs. Sham VEH). Individual data points represented as • males, Δ females.” The authors apologize for these errors and state that they do not change the scientific conclusions of the article in any way. The original article has been updated. Copyright © 2025 Lipari, Galfano, Venkatesh, Grezenko, Sandoval, Manfredsson and Bishop.