Frontiers Corrigendum Template for Authors. Original title article: The effects of chemogenetic targeting of serotonin-projecting pathways on L-DOPA-induced dyskinesia and psychosis in a bilateral rat model of Parkinson's disease.

Natalie Lipari ^1* Ashley Galfano ¹ Shruti Venkatesh ¹ Han Grezenko ² Ivette Sandoval ² Fredric P Manfredsson ² Christopher R. Bishop ^1*

• ¹ Binghamton University, Binghamton, United States
• ² Barrow Neurological Institute (BNI), Phoenix, Arizona, United States

• please read through all the templates before choosing • pick the most relevant text template(s) from the following page and delete all others.• edit the text as necessary, ensuring that the original incorrect text is included for the record, please see the below. • please do not use any extra formatting when editing the templates, and only modify the red text unless absolutely necessary • submit to Frontiers following the instructions on this page.When the original text contained incorrect information, to preserve the scientific record, please include that text when editing the below templates. For example:There was a mistake in the Funding statement, an incorrect number was used. The correct number is "2015C03Bd051.". The publisher apologizes for this mistake.The original version of this article has been updated.In the published article, there was a mistake in the Funding statement. The funding statement for the Key Development Project of the Department of Science and Technology was displayed as "2015CBd051". The correct statement is "Key Development Project of Department of Science and Technology (2015C03Bd051).'' Template continues on the next page PAGE \* Arabic \* MERGEFORMAT 3In the published article, there was an error in the legend for [Figure 2: Establishment of motor deficits and development of Levodopa-induced dyskinesia (LID) in a bilateral 6hydroxydopamine (6-OHDA) rat model of Parkinson's disease.] as published. [The legend for Figure 2 is incorrect]. The corrected legend 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 independentsamples 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,  Females.]The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.In the published article, there was an error in the legend for [Figure 3: The effects of bilateral 6hydroxydopamine (6-OHDA) lesion and history of levodopa (LD) treatment on prepulse inhibition (PPI)] as published. [The legend for Figure 3 is incorrect]. The corrected legend appears below.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) x 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) x 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,  Females.] PAGE \* Arabic \* MERGEFORMAT 3In the published article, there was an error in the legend for [Figure 4: Effects of acute compound 21 (C21) on levodopa-induced dyskinesia (LID), and motor performance in levodopa (LD)treated animals.] as published. [The legend for Figure 4 is incorrect]. The corrected legend 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 hr 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 nonparametric 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)) x 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 x Treatment interaction). Individual data points represented as • Males,  Females.]In the published article, there was an error in the legend for [Figure 5: The effects of acute compound 21 (C21) treatment on prepulse inhibition (PPI).] as published. [The legend for Figure 5 is incorrect]. The corrected legend 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) x 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,  Females.] PAGE \* Arabic \* MERGEFORMAT 3In the published article, there was an error in the legend for [Figure 6: Loss of tyrosine hydroxylase (TH) immunoreactive neurons following bilateral 6-hydroxydopamine (6-OHDA) lesion and chronic treatment.] as published. [The legend for Figure 6 is incorrect]. The corrected legend 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,  Females.] End of template, if you would like to request a correction for a reason not seen here, please contact the journal's Editorial Office