Institution: | * Department of Pharmacology. Warner Lambert/Parke-Davis Pharmaceutical Research, Ann Arhor, MI 48105, USA ? Departments of Neuroscience. Pharmacology and Experimental Therapeutics, and Psychiatry and Behavioral Sciences, John Hopkins School of Medicine, Baltimore, MD 21205, USA ? Laboratory of Bioorganic Chemistry, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20205, USA ¶ Department of Environmental Health Sciences, Johns Hopkins School of Hygiene, Baltimore, MD 21205, U.S.A. |
Abstract: | and 3H]-1,3-diethyl-8-phenylxanthine label the A1 subtype of adenosine receptor in brain membranes. The affinities of methylxanthines in competing for A1 adenosine receptors parallel their potencies as locomotor stimulants. The adenosine agonist N6-(-phenylisopropyl) adenosine is a potent locomotor depressant. Both diazepam and cause locomotor stimulation in a narrow range of subdepressant doses. Combined stimulant doses of the two agents depress motor activity, as do larger doses of either one, given separately.Evidence supporting and against the hypothesis that some of the actions of benzodiazepines are mediated via the adenosine system is reviewed. A number of compounds interact with both systems, probably because of physico-chemical similarities between adenosine and diazepam. It is concluded that of the four classic actions of benzodiazepines, the sedative and muscle relaxant (but not anxiolytic or anticonvulsant) actions could possibly be mediated by adenosine. |