Behavioural Neuroscience Poster Session
Nakamura, Y. (Department of Pharmacolocgy, Okayama University, Japan)
Kamei, C. (Department of Pharmacology, Faculty of Pharmaceutical Sciences, Okayama University, Japan)
The role of histamine on compound 48/80-induced skin reactions was studied in mice. Subcutaneous injection of compound 48/80 into the rostral back of the mouse elicited dose-dependently the scratching behavior and skin vasal permeability of the injected site. Moreover, chronic treatment of compound 48/80 resulted in a significant decrease in the scratching behavior and histamine contents of the injected site. Classical histamine H1-receptor antagonists such as diphenhydramine and chlorpheniramine caused a dose-related inhibition of compound 48/80-induced scratching behavior and vasal permeability. Histamine H1-receptor antagonists having antiallergic activity (an inhibition of mast cell degranulation), such as azelastine and non-sedative histamine H1-receptor antagonists such as terfenadine, epinastine and astemizole, also showed a relatively potent effect. On the other hand, the effect of tranilast, antiallergic drug without histamine H1-receptor antagonistic activity, was extremely weak. Diazepam had weak or no depressant effects on compound 48/80-induced scratching behavior. These results suggest that the histamine released from skin mast cells play an important role in the generation of compound 48/80-induced scratching behavior and vasal permeability in mice.
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|Sugimoto, Y.; Nakamura, Y.; Kamei, C.; (1998). Involvement of histamine on compound 48/80-induced skin reactions in mice. 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/behavneuro/sugimoto0283/index.html|
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