CONICET | Buscador de Institutos y Recursos Humanos

There is evidence that prenatal exposure to cannabinoids agonists induce long-term alterations in the opioid system. Here and at previous studies we compared the effect of prenatal exposure to a cannabinoid agonist WIN 55,212-2 (WIN) in a genotype model, CB1 receptor knockout mice (CB1 KO).In previous studies from our laboratory performed in adolescent CB1 KO mice, we reported a decrease in the expression of naloxone (NAL) precipitated morphine (MOR) withdrawal syndrome compared to their wild-type (WT) littermates, both groups prenatally treated with vehicle (VEH). In the same studies we found a decrease in the expression of MOR withdrawal syndrome in the WT prenatally treated with WIN compared to the WT prenatally treated with VEH, and found no differences between WT and CB1 KO both groups prenatally treated with WIN.The aim of the present study was to evaluate the effect of the prenatal exposure to the cannabinoid agonist WIN in c-Fos expression of certain brain areas of MOR withdrawn CB1 KO and WT adolescent mice.Pregnant female CB1 KO and WT mice received WIN (0.75 mg/kg, s.c.) or vehicle (VEH) once daily from 5th to 15th gestational day. From 25th postnatal day forward, mice were treated for 9 days with MOR (2 mg/kg, i.p.) or saline (SAL) twice daily. On the tenth day, the animals received NAL (6 mg/kg, i.p.) or SAL 60 min after the last injection and 30 min after precipitating the withdrawal, mice were perfused with a PFA 4% solution and brains were removed and coronal frozen sections were made at 30 μm on a freezing microtome to perform the c-Fos immunohistochemistry (IHC).WT but not KO adolescent mice prenatally treated with VEH show a c-Fos expression decrease during MOR withdrawal syndrome in Cg (p