The inhibition of cocaine-induced locomotor activity by CART 55-102 is lost after repeated cocaine administration

• Type of Material: Article
• Authors: Martin O. Job, Emory University; Li L. Shen, Emory University; Michael Kuhar, Emory University
• Language: English
• Date: 2013-08-29
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2013 The Authors.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.neulet.2013.06.039
• Title of Journal or Parent Work: Neuroscience Letters
• ISSN: 0304-3940
• Volume: 550
• Start Page: 179
• End Page: 183
• Grant/Funding Information: It was also supported by DA 015040, DA 15162 and the Georgia Research Alliance.; This project was funded by the National Center for Research Resources P51RR165 and is currently supported by the Office of Research Infrastructure Programs/OD P51OD11132.
• Keywords: Chronic; Science & Technology; EXPRESSION; Acute; Cocaine; Neurosciences & Neurology; Life Sciences & Biomedicine; D1; INJECTION; INCREASES; MESSENGER-RNA; Neurosciences; DOPAMINE-RECEPTORS; RAT NUCLEUS-ACCUMBENS; AMPHETAMINE; CART peptide; BODY-WEIGHT; CART 55-102; REGULATED TRANSCRIPT PEPTIDE
• Research Categories: Biology, Neuroscience

Abstract

CART peptide is known for having an inhibitory effect on cocaine- and dopamine-mediated actions after acute administration of cocaine and dopamine. In this regard, it is postulated to be a homeostatic, regulatory factor on dopaminergic activity in the nucleus accumbens (NAc). However, there is no data on the effect of CART peptide after chronic administration of cocaine, and this study addresses this. It was found that CART peptide blunted cocaine-induced locomotion (LMA) after acute administration of cocaine, as expected, but it did not affect cocaine-mediated LMA after chronic administration of cocaine. The loss of CART peptide's inhibitory effect did not return for up to 9 weeks after stopping the repeated cocaine administration. It may not be surprising that homeostatic regulatory mechanisms in the NAc are lost after repeated cocaine administration, and that this may be a mechanism in the development of addiction.