Combined effects of buprenorphine and an alternative nondrug reinforcer on phencyclidine self-administration in rhesus monkeys.

Six rhesus monkeys self-administered orally delivered phencyclidine (PCP; 0.35 mg/ml) with saccharin (0.3 or 0.03 % wt/vol) or water under concurrenl fixed-ralio (FR) schedules. During daily 3-hr sessions, subjects had concurrent access to liquids: PCP versus water, PCP versus saccharin. or saccharin versus water. The FR of both liquids was varied (4, 8, 16, 32, and 64) in nonsystematic order and when behavior was stable at each FR, buprenorphine (0.005 mg/kg) was injected intramuscularly for 5 days. Buprenorphine treatment decreased PCP deliveries by 16–65% across the range of FR values when compared with the no-treatment baseline, and concurrent saccharin reduced PCP deliveries from 34 to 63%. Combining buprenorphine treatment and concurrent availability of saccharin produced decreases in PCP deliveries of 70–87% from the no-trealmenl baseline across the FR values. Greater reductions were found at the highest FR values. Pmax values were shifted to the left under all treatment conditions, suggesting that the reinforcing efficacy of the drug was reduced. These findings suggest that pharmacological and behavioral treatments produce additive reductions in drug self-administration. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The effects of restraint stress on voluntary ethanol consumption in rats.

Sixty Wistar rats (Rattus norvegicus) were assigned to 4 groups of 15 rats each: ethanol stress (ES), ethanol no-stress (EN), isocaloric stress (IS) and isocaloric no-stress (IN). The effect of restraint stress on daily intake of ethanol and a 0.72% solution of glucose was examined in an ABA design (stress-no stress-stress). During the stress phases, 2 groups were subjected to daily 15-min restraint stress, whereas 2 groups were placed in different cages for 15 min as a control. All 4 groups were then given 6-hr access to their assigned liquid alone for 4 days followed by a choice between their assigned liquid and water on the 5th day. The ES group significantly increased their ethanol intake (g/kg) compared to the EN group on choice days but not on forced days. Percentage preference for ethanol was significantly greater and increased at a faster rate over the 75-day testing period compared with the EN group. However, total ethanol consumption (g/kg) and percentage preference did not vary as a function of phase. It is notable that the effects of restraint stress on ethanol self-administration persisted even after the stress schedule was removed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Prenatal and lactational exposure to methylmercury affects select parameters of mouse cerebellar development

Animal studies of the neuropathological effects of prenatal methylmercury (MeHg) seldom use regimens that represent environmental exposures. While acute administration of high doses of MeHg to developing rodents can model some of the outcomes MeHg produces in the human cerebellum, their long-term relevance to cerebellar development is unknown. The present study was undertaken to determine the effect of chronic dietary exposure to MeHg. Pregnant mice were exposed throughout gestation to 0.0 or 4.0 ppm methylmercury in their drinking water. Postpartum exposure of pups and lactating dams continued to postnatal day (PND) 30. On PND7, 14, 21, and 30, several morphometric indices of cerebellar cortex development, as well as blood and brain levels of total Hg, were measured in pairs of male and female littermates. No signs of overt toxicity were observed in the dams or offspring. Blood and brain levels of total Hg were highest in the exposed PND7 offspring and fell throughout the sampling period despite continued exposure. In a region of molecular layer in the anterodorsal lobe, MeHg exposure reduced the density of migrating cells in PND7 offspring. Molecular layer widths were reduced in PND30 offspring. In a region of the inferior lobe of PND7 offspring, MeHg exposure reduced external granular layer widths and decreased the density of migrating cells in the molecular layer. However, MeHg did not affect cerebellar cortex development in the central lobe, suggesting a regional sensitivity to chronic, low-level MeHg exposure during development.