am-356 and 1-3-dipropyl-8-cyclopentylxanthine

am-356 has been researched along with 1-3-dipropyl-8-cyclopentylxanthine* in 1 studies

Other Studies

1 other study(ies) available for am-356 and 1-3-dipropyl-8-cyclopentylxanthine

Article	Year
Adenosine A2a blockade prevents synergy between mu-opiate and cannabinoid CB1 receptors and eliminates heroin-seeking behavior in addicted rats. Proceedings of the National Academy of Sciences of the United States of America, 2006, May-16, Volume: 103, Issue:20 Relapse is the most serious limitation of effective medical treatment of opiate addiction. Opiate-related behaviors appear to be modulated by cannabinoid CB1 receptors (CB1) through poorly understood cross-talk mechanisms. Opiate and CB1 receptors are coexpressed in the nucleus accumbens (NAc) and dorsal striatum. These regions also have the highest density of adenosine A2a receptors (A2a) in the brain. We have been investigating the postsynaptic signaling mechanisms of mu-opiate receptors (MORs) and CB1 receptors in primary NAc/striatal neurons. In this article, we present evidence that MOR and CB1 act synergistically on cAMP/PKA signaling in NAc/striatal neurons. In addition, we find that synergy requires adenosine and A2a. Importantly, an A2a antagonist administered either directly into the NAc or indirectly by i.p. injection eliminates heroin-induced reinstatement in rats trained to self-administer heroin, a model of human craving and relapse. These findings suggest that A2a antagonists might be effective therapeutic agents in the management of abstinent heroin addicts. Topics: Adenosine A2 Receptor Antagonists; Analgesics, Opioid; Animals; Arachidonic Acids; Behavior, Animal; Corpus Striatum; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Drug Synergism; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enzyme Activation; Gene Expression Regulation; Heroin Dependence; Humans; Male; Neurons; Nucleus Accumbens; Rats; Rats, Sprague-Dawley; Receptor, Adenosine A2A; Receptor, Cannabinoid, CB1; Receptors, Opioid, mu; Self Administration; Signal Transduction; Theobromine; Xanthines	2006

Article

Year

Adenosine A2a blockade prevents synergy between mu-opiate and cannabinoid CB1 receptors and eliminates heroin-seeking behavior in addicted rats.

Proceedings of the National Academy of Sciences of the United States of America, 2006, May-16, Volume: 103, Issue:20

Relapse is the most serious limitation of effective medical treatment of opiate addiction. Opiate-related behaviors appear to be modulated by cannabinoid CB1 receptors (CB1) through poorly understood cross-talk mechanisms. Opiate and CB1 receptors are coexpressed in the nucleus accumbens (NAc) and dorsal striatum. These regions also have the highest density of adenosine A2a receptors (A2a) in the brain. We have been investigating the postsynaptic signaling mechanisms of mu-opiate receptors (MORs) and CB1 receptors in primary NAc/striatal neurons. In this article, we present evidence that MOR and CB1 act synergistically on cAMP/PKA signaling in NAc/striatal neurons. In addition, we find that synergy requires adenosine and A2a. Importantly, an A2a antagonist administered either directly into the NAc or indirectly by i.p. injection eliminates heroin-induced reinstatement in rats trained to self-administer heroin, a model of human craving and relapse. These findings suggest that A2a antagonists might be effective therapeutic agents in the management of abstinent heroin addicts.

Topics: Adenosine A2 Receptor Antagonists; Analgesics, Opioid; Animals; Arachidonic Acids; Behavior, Animal; Corpus Striatum; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Drug Synergism; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enzyme Activation; Gene Expression Regulation; Heroin Dependence; Humans; Male; Neurons; Nucleus Accumbens; Rats; Rats, Sprague-Dawley; Receptor, Adenosine A2A; Receptor, Cannabinoid, CB1; Receptors, Opioid, mu; Self Administration; Signal Transduction; Theobromine; Xanthines

2006