Neuropharmacology Poster Session
Kraus, M. (Department of Pharmacology and Toxicology, University of Innsbruck, Austria)
Tran, MH. (Department of Biochemistry-Pharmacology, Ho Chi Minh City, Vietnam)
Philippu, A. (Department of Pharmacology and Toxicology, University of Innsbruck, Austria)
The anterior hypothalamus of anaesthetized rats was superfused through a push-pull cannula either with drugs which influence extracellular adenosine concentration, or with ligands of adenosine receptors and the released histamine was determined in the superfusate by HPLC. Superfusion with the inhibitor of adenosine deaminase EHNA (100 and 200 Ámol/l) or with the inhibitor of adenosine transport dipyridamole (50 Ámol/l)increased histamine release. These findings indicate that endogenous adenosine released in the synaptic cleft stimulates histamine release. Superfusion of the hypothalamus with the A1 adenosine receptor agonist CPA (50 Ámol/l) enhanced, whereas the A1 receptor antagonist CPT (50 Ámol/l)and the A2 receptor agonist CPCA (50 Ámol/l) decreased histamine release rate. The A2 receptor antagonist DMPX (50 Ámol/l) augmented the release of the amine. Hence, A1 receptor activation increases, while activation of A2 receptors reduces histamine release in the hypothalamus. The effects obtained with the adenosine receptor antagonists indicate that histamine release is permanently modulated by A1, as well as A2 receptors. Stimulation of histamine release by A1 receptors seems to overrule inhibition of histamine outflow by A2 receptors, since elevation of extracellular adenosine level by EHNA or dipyridamole enhances histamine release.
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|Prast, H.; Kraus, M.; Tran, MH.; Philippu, A.; (1998). Modulation of histamine release in the hypothalamus by adenosine. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Available at URL http://www.mcmaster.ca/inabis98/neuropharm/prast0269/index.html|
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