Cardiovascular and Subjective Effects of the Novel Adenosine A2A ReceptorAntagonist SYN115 in Cocaine Dependent IndividualsLane SD1,2*, Green CE3, Steinberg JL1, Ma L1, Schmitz JM1,2, Rathnayaka N1, Bandak SD4, Ferre S5 and Moeller FG1,2
- *Corresponding Author:
- S.D. Lane BBSB 1312
Center for Neurobehavioral Research on Addiction
University of Texas Health Science Center at Houston
1941 East Road, Houston, TX 77054, USA
E-mail: [email protected]
Received February 20, 2012; Accepted March 26, 2012; Published March 28, 2012
Citation: Lane SD, Green CE, Steinberg JL, Ma L, Schmitz JM, et al. (2012) Cardiovascular and Subjective Effects of the Novel Adenosine A2A Receptor Antagonist SYN115 in Cocaine Dependent Individuals. J Addict Res Ther S1:009. doi:10.4172/2155-6105.S1-009
Copyright: © 2012 Lane SD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
A2A receptor antagonists have been proposed as therapeutic tools for dopaminergically-relevant diseases, including Parkinson's disease and substance dependence. The acute subjective and cardiovascular effects of a novel, selective adenosine A2A receptor antagonist (SYN115) were examined. Across an 8-hour experimental testing day, 22 nontreatment seeking cocaine-dependent subjects received either placebo capsules (PO) at both the AM and PM dosing times (Plc/Plc, N = 9), or placebo in the AM and 100 mg SYN115 in the PM (Plc/SYN115, N =13). Cardiovascular measures (HR, BP) were obtained across the test day, and subjective effects (ARCI, VAS) were obtained once before and once after the AM and PM doses (four time points total). There were no between-group effects on cardiovascular function, however subjective effects consistent with stimulation were observed on the VAS scales in the SYN115 group. In cocaine-dependent subjects, SYN115 may produce stimulant-like effects through a unique mechanism of action. Due to known monoamine dysfunction related to chronic cocaine use, these effects may be specific to this population relative to healthy control or other patient populations.