Abstract
We studied whether interactions between the presynaptic histamine H3 and prostaglandin EP3 receptors on the noradrenergic neurons of the mouse brain cortex occur. Cerebral cortex slices from the mouse (and, in few experiments, from the rat) were preincubated with [3H]noradrenaline and then superfused with a physiological salt solution. Tritium overflow was evoked electrically, either at 0.3 or 3 Hz (2 min) (standard stimulation protocol) or at 100 Hz (eight pulses) (stimulation protocol under which almost no activation of the presynaptic alpha2-adrenoceptors by endogenous noradrenaline occurs). In another set of experiments, Ca2+ ions were introduced into Ca2+-free K+-rich medium containing tetrodotoxin to evoke tritium overflow. The electrically-evoked tritium overflow (0.3 Hz) was inhibited by histamine or the H3 receptor agonist imetit, acting via H3 receptors. and by prostaglandin E2 or the EP3 receptor agonist sulprostone, acting via EP3 receptors. When histamine or imetit was given first (at concentrations causing the maximum effect at H3 receptors), the effect of prostaglandin E2 on the evoked tritium overflow was attenuated by 5-10%. When prostaglandin E2 or sulprostone was given first (at concentrations causing the max...Continue Reading
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Citations
Jun 3, 2008·Neurotoxicity Research·Przemyslaw NowakRyszard Brus
Jan 14, 2003·European Journal of Pharmacology·Kunihiko YokotaniShoshiro Okada
Mar 2, 1999·British Journal of Pharmacology·C MazenotD Godin-Ribuot
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