caa a22 4500 469079428 CHVBK 20180323132945.0 cr unu---uuuuu 170328e19920401xx s 000 0 eng 10.1007/BF00176630 doi (NATIONALLICENCE)springer-10.1007/BF00176630 Histamine H3A receptor-mediated inhibition of noradrenaline release in the mouse brain cortex [Elektronische Daten] [E. Schlicker, A. Behling, G. Lümmen, M. Göthert] Summary: Mouse brain cortex slices preincubated with 3H-noradrenaline were superfused with physiological salt solution containing desipramine plus a drug with α2-adrenoceptor antagonist properties, and the effects of histamine receptor ligands on the electrically (0.3 Hz) evoked tritium overflow were studied. The evoked overflow (from slices superfused with phentolamine) was inhibited by histamine (pIC35 6.53), the H3 receptor agonist R-(−)-α-methylhistamine (7.47) and its S-(+)-enantiomer (5.82) but not influenced by the H1 receptor agonist 2-(2-thiazolyl)-ethylamine 3.2 μmol/l and the H2 receptor agonist dimaprit 10 μmol/l. The inhibitory effect of histamine was not affected by the H1 receptor antagonist dimetindene 1 μmol/l and the H2 receptor antagonist ranitidine 10 μol/l. The concentration-response curve of histamine (determined in the presence of rauwolscine) was shifted to the right by the H3 receptor antagonists thioperamide (apparent pA2 8.67), impromidine (7.30) and burimamide (6.82) as well as by dimaprit (6.16). The pA2 values of the four drugs were compared with their affinities for H3A and H3B binding sites in rat brain membranes (West et al. 1990 Mol Pharmacol 38:610); a significant correlation was obtained for the H3A, but not for the H3B sites. The results suggest that noradrenaline release in the mouse brain cortex is inhibited by histamine via H3A receptors and that dimaprit is an H3 receptor antagonist of moderate potency. Springer-Verlag, 1992 H3A receptors nationallicence Noradrenaline release nationallicence Dimaprit nationallicence Presynaptic receptors nationallicence Mouse brain cortex slices nationallicence Schlicker E. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut Behling A. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut Lümmen G. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut Göthert M. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/4(1992-04-01), 489-493 0028-1298 345:4<489 1992 345 210 https://doi.org/10.1007/BF00176630 text/html Onlinezugriff via DOI 1 brief-communication jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00176630 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Schlicker E. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut NATIONALLICENCE 700 1- Behling A. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut NATIONALLICENCE 700 1- Lümmen G. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut NATIONALLICENCE 700 1- Göthert M. Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstrasse 2b, W-5300, Bonn 1, Germany aut NATIONALLICENCE 773 0- Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/4(1992-04-01), 489-493 0028-1298 345:4<489 1992 345 210 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer