Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2014 Jun 17;4(6):e401. doi: 10.1038/tp.2014.43

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2014 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

PMC Copyright notice

Only the preferential D₃R agonist, PD-128907, reverses the instrumental deficit induced by 6-OHDA SNc lesions. Evolution of operant sucrose (2% in water) self-administration performances, under a fixed ratio 1 (FR1) schedule of reinforcement, in sham-operated (white chips) and lesioned (black chips) animals, during the eight instrumental sessions. Subchronic administration of PD-128907 (0.1 and 0.15 mg kg⁻¹), but not of SKF-38393 (2.5 and 3.5 mg kg⁻¹) or sumanirole (0.1 and 0.15 mg kg⁻¹), improved the instrumental performances of 6-OHDA-lesioned rats. Dot lines represented the mean of the instrumental performances of the three last FR1 sessions of vehicle-treated sham animals. *P<0.05; **P<0.01; ***P<0.001, sham-operated versus lesioned within the same treatment (n=8–21 per group). 6-OHDA, 6-hydroxydopamine; PD, Parkinson's disease; SNc, substantia nigra pars compacta.