Effects of cannabinoids infused into the dorsal hippocampus upon memory formation in 3-days apomorphine-treated rats.
In the present study, the effects of intra-dorsal hippocampus (intra-CA1) injection of cannabinoid receptor agents on memory formation have been investigated in 3-days apomorphine-treated rats. Step-through inhibitory avoidance task of memory has been used to examine retrieval of memory formation, 24h after training. Apomorphine was injected subcutaneously (S.C.), once daily for 3-days followed by 5 days free of the apomorphine before training. Bilateral post-training intra-CA1 infusions of the non selective CB1-CB2 receptor agonist, WIN55,212-2 (0.1, 0.25 and 0.5 microg/rat), dose-dependently shortened the step-through latency, suggesting amnesia by the drug, whereas bilateral post-training intra-CA1 micro-injections of the selective CB1 receptor antagonist, AM251 (25, 50 and 100 ng/rat), did not affect memory formation. Intra-CA1 infusions of AM251 and WIN55,212-2, two min apart, modify the WIN55,212-2-induced reduction of step-through latency. Furthermore, the deleterious effect of WIN55,212-2 (0.25 microg/rat) was completely abolished in rats previously given apomorphine (0.5 and 1 mg/kg/day, S.C.) for 3 days. This prevention of WIN55,212-2-induced amnestic-like effect was counteracted by the dopamine D2 receptor antagonist, sulpiride (0.25, 0.5 and 1 mg/kg/day x 3-days, S.C.), administered 30 min before each injection of apomorphine (0.5 mg/kg/day x 3-days, S.C.). The D1 receptor antagonist, SCH 23390 (0.01, 0.02, 0.07 and 0.1 mg/kg/day x 3-days, S.C.), was ineffective in this respect. The results suggest that subchronic apomorphine treatment may induce dopamine D2 receptor sensitization, which in turn prevented amnesia induced by WIN55,212-2.
Nasehi
Mohammad
M
Department of Biology, Faculty of Basic Sciences, Islamic Azad University, Garmsar Branch, Semnan, Iran.
Sahebgharani
Mousa
M
Haeri-Rohani
Ali
A
Zarrindast
Mohammad Reza
MR
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D001362:Avoidance Learning / Q000187:drug effects; D001552:Benzazepines / Q000494:pharmacology; D048588:Benzoxazines / Q000008:administration & dosage / Q000494:pharmacology; D002186:Cannabinoids / Q000008:administration & dosage / Q000494:pharmacology*; D018491:Dopamine Agonists / Q000494:pharmacology*; D018492:Dopamine Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006624:Hippocampus / Q000187:drug effects*; D008297:Male; D008568:Memory / Q000187:drug effects*; D011939:Mental Recall / Q000187:drug effects; D009025:Morpholines / Q000008:administration & dosage / Q000494:pharmacology; D009281:Naphthalenes / Q000008:administration & dosage / Q000494:pharmacology; D009483:Neuropsychological Tests; D010880:Piperidines / Q000008:administration & dosage / Q000494:pharmacology; D011720:Pyrazoles / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D043884:Receptor, Cannabinoid, CB1 / Q000819:agonists / Q000037:antagonists & inhibitors; D043885:Receptor, Cannabinoid, CB2 / Q000819:agonists; D013469:Sulpiride / Q000008:administration & dosage / Q000494:pharmacology; D013997:Time Factors
D001552:Benzazepines; D048588:Benzoxazines; D002186:Cannabinoids; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D009025:Morpholines; D009281:Naphthalenes; D010880:Piperidines; D011720:Pyrazoles; D043884:Receptor, Cannabinoid, CB1; D043885:Receptor, Cannabinoid, CB2; C534628:SCH 23390; C103505:AM 251; C070417:(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone; D013469:Sulpiride; D001058:Apomorphine