Article date: December 1988
By: S.J. Hill, R.M. Straw in Volume 95, Issue 4, pages 1213-1219
Depolarization of rat cerebral cortical slices, prelabelled with [3H]‐histidine, in high potassium (40 mM KCl) medium stimulated the release of [3H]‐histamine. The K+‐evoked release of [3H]‐histamine was attenuated by incubation in calcium‐free medium and prevented by prior incubation of brain slices with the selective histidine decarboxylase inhibitor S‐(α)‐fluoromethylhistidine.
The K+‐evoked release of [3H]‐histamine was significantly (P < 0.001) reduced following stimulation of histamine H3‐receptors with R‐(α)‐methylhistamine (1 μm) and this effect was antagonized by the H3‐antagonist thioperamide (1 μm).
Noradrenaline and the α2‐selective adrenoceptor agonists clonidine and UK‐14,304 inhibited the K+‐evoked release of [3H]‐histamine in a concentration‐dependent manner yielding EC50 values of 2.5, 0.8 and 1.2 μm, respectively. However, the maximum response to clonidine was only 52 ± 8% of that obtained with noradrenaline.
The inhibitory effect of noradrenaline was antagonized by the non‐selective α‐antagonist phentolamine and by the selective α2‐antagonists yohimbine and idazoxan. However, the response to noradrenaline was not inhibited by the α1‐antagonist prazosin at concentrations up to 1 μm.
These results suggest that both histamine H 3‐receptors and α2‐adrenoceptors are present on histamine‐containing nerve terminals in rat cerebral cortex and can exert an inhibitory influence on neurotransmitter release.
Depolarization of rat cerebral cortical slices, prelabelled with [3H]‐histidine, in high potassium (40 mM KCl) medium stimulated the release of [3H]‐histamine. The K+‐evoked release of [3H]‐histamine was attenuated by incubation in calcium‐free medium and prevented by prior incubation of brain slices with the selective histidine decarboxylase inhibitor S‐(α)‐fluoromethylhistidine.
The K+‐evoked release of [3H]‐histamine was significantly (P < 0.001) reduced following stimulation of histamine H3‐receptors with R‐(α)‐methylhistamine (1 μm) and this effect was antagonized by the H3‐antagonist thioperamide (1 μm).
Noradrenaline and the α2‐selective adrenoceptor agonists clonidine and UK‐14,304 inhibited the K+‐evoked release of [3H]‐histamine in a concentration‐dependent manner yielding EC50 values of 2.5, 0.8 and 1.2 μm, respectively. However, the maximum response to clonidine was only 52 ± 8% of that obtained with noradrenaline.
The inhibitory effect of noradrenaline was antagonized by the non‐selective α‐antagonist phentolamine and by the selective α2‐antagonists yohimbine and idazoxan. However, the response to noradrenaline was not inhibited by the α1‐antagonist prazosin at concentrations up to 1 μm.
These results suggest that both histamine H 3‐receptors and α2‐adrenoceptors are present on histamine‐containing nerve terminals in rat cerebral cortex and can exert an inhibitory influence on neurotransmitter release.
DOI: 10.1111/j.1476-5381.1988.tb11758.x
View this article