Cocaine reward and reinstatement in adolescent versus adult rodents.

Adolescence is a critical juncture when initiation of drug use intersects with profound developmental changes in the brain. Adolescent drug use increases the risk to develop substance use disorders (SUDs) later in life, but the mechanisms that confer this vulnerability are not understood. SUDs are defined by cycles of use, abstinence, and relapse. Intense craving during drug-free periods is often triggered by cues and environmental contexts associated with previous use. In contrast to our understanding of stimuli that elicit craving and relapse in adults, the behavioral processes that occur during periods of abstinence and relapse in adolescents are poorly understood. The current mini-review will summarize findings from preclinical rodent studies that used cocaine conditioned place preference and operant cocaine self-administration to examine subsequent effects on reward, relapse and incubation of craving.

Effects of moderate ethanol consumption as a function of n-6:n-3 dietary ratio on lipid profile, inflammation, and liver function in mice.

Objective: It is critical to understand how moderate ethanol exposure interacts with dietary components such as essential fatty acids to influence inflammatory processes underlying CVD pathogenesis. The purpose of this study was to examine the effects of moderate ethanol consumption and dietary n-6:n-3 fatty acid composition on markers associated with CVD in mice. Methods: Twenty-three C57BL/6J mice consumed an 18% ethanol solution or 26.9% maltose dextrin solution (isocaloric control) for 12 weeks. Within each group, the mice were fed either a high n-6 (n-6:n-3 = 50:1) diet or a balanced n-3 (n-6:n-3 = 1:1) diet ad libitum. Following the exposure period, serum samples were analyzed to assess lipid profile, inflammatory markers, antioxidant capacity, DNA damage, and liver function enzyme activity. Results: The control group gained more weight than the ethanol group (P = 0.020). In ethanol-exposed mice, HDL was significantly increased (P = 0.009). C-reactive protein (CRP; P < 0.001), high mobility group box 1 protein (HMGB1; P = 0.011), 8-oxo-deoxyguanosine (8-oxo-dG; P = 0.019), ALT (P = 0.002) and AP (P = 0.021) were lower in the ethanol group. There was a significant main effect of the n-3 diet on total antioxidant capacity (TAC; P < 0.001) and 8-oxo-dG (P = 0.047). Conclusion: These findings indicate that moderate ethanol consumption and a balanced n-6:n-3 diet improve several inflammatory and lipid markers associated with CVD. Observed differences in weight gain between groups should be considered when interpreting these results.