Cannabinoids: effects on behaviour and leukocyte phagocytosis
Autoři | |
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Rok publikování | 2002 |
Druh | Článek ve sborníku |
Konference | Abstracts of Workshop: Psychopharmacology of Cannabis and Ecstasy |
Fakulta / Pracoviště MU | |
Citace | |
Obor | Farmakologie a lékárnická chemie |
Klíčová slova | cannabinoids; cannabinoid CB1 and CB2 receptors; social behaviour; leukocyte phagocytosis; "i.v. self-administration"; mice; rats |
Popis | The study shows that both agonistic and antagonistic manipulation with cannabinoid CB1 as well as CB2 receptor caused changes in social behaviour in mice. Mixed CB1,2 agonists produced biphasic effects - stimulation of aggressive behaviour in timid mice at low doses and inhibition of aggressive activities in aggressive mice at high doses. Inhibitory influence on aggressive behaviour in aggressive mice was present also after all tested doses of selective CB1 agonist, was lower after CB2 agonist and was not apparent after administration of CB1 antagonist. Pro-aggressive effects in timid mice were elicited besides CB1,2 agonists also by both, CB1 and CB2 agonist. The effects of cannabinoid receptor ligands on leukocyte phagocytosis resemble those observed in behavioural studies as CB1,2 agonists produced biphasic influence - stimulation and suppression of phagocytic activity at low and high doses, respectively. Such effects were apparent also after administration of selective CB2 agonist but surprisingly to some extent of smaller intensity. Selective antagonists of both CB1 and CB2 receptor showed only inhibitory effect on leukocyte phagocytosis. Calcium channel blocker verapamil when combined with anandamide antagonised both stimulatory and inhibitory effects of the cannabinoid on social behaviour and on leukocyte phagocytosis, too. Our experiments carried out on methamphetamine dependent rats using a nose-poking response-like as operandum confirmed the functional interactions between cannabinoids and i.v. self-administered methamphetamine. There was found a significant influence of CB1 antagonist on inhibition of methamphetamine intake. |
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