Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P21554 (cannabinoid receptor)
 3,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although still very preliminary, these studies exemplify how metabolic brain measurements can address questions of relevance in the investigation of drugs of addiction such as: 1. Mechanisms of drug toxicity, i.e., vascular pathology demonstrated from chronic use of cocaine. 2. Neurotransmitters that may be involved in the pharmacological actions of drugs, i.e., alcohol and the benzodiazepine-Gaba receptor complex, marijuana, and the cannabinoid receptor. 3. Mechanisms of drug withdrawal, i.e., hyperresponsivity of the brain to alcohol in the alcoholic, possibly as a consequence of increased sensitivity of the benzodiazepine-Gaba receptor complex. 4. Knowledge about brain function, i.e., the relation between activation of the cerebellum by marijuana and alcohol and the mood-changing effects of these drugs, suggests that the cerebellum may play a role in the mood disturbing actions seen with these drugs (a role which is different from the classical one which associates the cerebellum to motor regulation). Future work will provide more definitive answers to the above questions and will similarly provide information about mechanisms of toxicity, addiction, withdrawal, and reinforcement of other drugs of abuse.
NIDA Res Monogr 1990
PMID:Metabolic studies of drugs of abuse. 187 84

The CB(1) cannabinoid receptor antagonist SR-141716A (Rimonabant) markedly diminishes the behavioral effects of opiates and nicotine and has been an important tool to ascertain the role of cannabinoid receptors in drug addiction. The present goal was to determine the less-explored interaction of SR-141716A and d-amphetamine in neurochemical and behavioral assays. Additionally, the effect of the substituents and substitution patterns on the phenyl ring located at the 5 position of SR-141716A (4-chlorophenyl), and of the CB(1)/CB(2) cannabinoid receptor agonist WIN-55,212-2, was determined. SR-141716A, AM-251 (4-iodophenyl) and NIDA-41020 (4-methoxyphenyl) did not alter amphetamine-evoked [(3)H]overflow from rat striatal slices preloaded with [(3)H]dopamine. MRI-8273-30-1 (4-fluorophenyl; 0.1-10 microM) attenuated amphetamine (3 microM)-evoked [(3)H]overflow, and MRI-8273-59 (3,4-dichlorphenyl; 0.01-10 microM) augmented amphetamine (0.3-3 microM)-evoked [(3)H]overflow. WIN-55,212-2 was without effect. In a locomotor activity experiment, SR-141716A and MRI-8273-30-1 did not alter amphetamine-induced hyperactivity. However, MRI-8273-59 (1-3 mg/kg) dose-dependently attenuated amphetamine (1 mg/kg)-induced hyperactivity. The present results suggest that SR-141716A is less efficacious to alter amphetamine effects than its reported efficacy to diminish the effects of opiates and nicotine. Modification of the 5-phenyl position of SR-141716A affords compounds that do interact with amphetamine in vitro and in vivo.
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PMID:Analogs of SR-141716A (Rimonabant) alter d-amphetamine-evoked [3H] dopamine overflow from preloaded striatal slices and amphetamine-induced hyperactivity. 1753 7