The H3 receptor is involved in cholecystokinin inhibition of food intake in rats

S Attoub, L Moizo, I Sobhani, JP Laigneau, MJM Lewin… - Life sciences, 2001 - Elsevier
S Attoub, L Moizo, I Sobhani, JP Laigneau, MJM Lewin, A Bado
Life sciences, 2001Elsevier
We investigated the peripheral effects of an H3-receptor agonist and an H3-receptor
antagonist (R) α-methylhistamine (Rα-MeHA) and thioperamide, respectively, on basal
feeding and the CCK8-induced inhibition of food intake in rat. Intraperitoneal injection of
thioperamide reduced food intake in a dose-dependent manner with maximal inhibition
(35%, P< 0.01 vs saline) at 3 mg/kg.(R) α-MeHA (0.3–3 mg/kg ip), an H3-receptor agonist
alone had no effect on feeding but reversed the thioperamide-induced inhibition of food …
We investigated the peripheral effects of an H3-receptor agonist and an H3-receptor antagonist (R)α-methylhistamine (Rα-MeHA) and thioperamide, respectively, on basal feeding and the CCK8-induced inhibition of food intake in rat. Intraperitoneal injection of thioperamide reduced food intake in a dose-dependent manner with maximal inhibition (35%, P<0.01 vs saline) at 3 mg/kg. (R)α-MeHA (0.3–3 mg/kg i.p.), an H3-receptor agonist alone had no effect on feeding but reversed the thioperamide-induced inhibition of food intake in a dose-dependent manner. The maximal feeding inhibitory dose of thioperamide (3 mg.kg i.p) increased by 40% and 22 % (P<0.01 vs saline) brain and stomach histamine contents, respectively. Histamine (0.3 – 6 mg/kg i.p.) and CCK-8 (3 – 30 μg/kg i.p) also inhibited food intake in a dose-dependent manner. Inhibition was 20% to 40% for histamine and 40% to 80% (P<0.01 vs saline) for CCK8. CCK-8 inhibition of feeding was increased by thioperamide and prevented by (R)α-MeHA in a dose-dependent way. In addition, CCK-8 did not reduce food intake if rats were pretreated with pyrilamine or ranitidine postsynaptic H1- and H2-receptor antagonists respectively. Our data suggest that the H3-receptor is involved in basal feeding. They also suggest that CCK satiety depends upon the release of histamine which acts on the H2- and H1-receptors, the final mediators of this effect.
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