Molecular mechanisms underlying sex and treatment-dependent differences in an animal model of cue-exposure therapy for cocaine relapse prevention.

Environmental enrichment combined with the glycine transporter-1 inhibitor Org24598 (EE+ORG) during cocaine-cue extinction (EXT) inhibited reacquisition of 1.0 mg/kg cocaine self-administration in male but not female rats in a previous investigation. In this investigation, we determined if this treatment benefit in males required EXT training and ascertained the molecular basis for the observed sex difference in treatment efficacy.

Assessment of Binge-Like Eating of Unsweetened vs. Sweetened Chow Pellets in BALB/c Substrains.

Binge eating disorder (BED) is defined as chronic episodes of consuming large amounts of food in less than 2 h. Binge eating disorder poses a serious public health problem, as it increases the risk of obesity, type II diabetes, and heart disease. Binge eating is a highly heritable trait; however, its genetic basis remains largely unexplored.

Role of preexisting inhibitory control deficits vs. drug use history in mediating insensitivity to aversive consequences in a rat model of polysubstance use.

Rationale: The nature and predictors of insensitivity to aversive consequences of heroin + cocaine polysubstance use are not well characterized.

Objectives: Translational methods incorporating a tightly controlled animal model of drug self-administration and measures of inhibitory control and avoidance behavior might be helpful for clarifying this issue.

Methods: The key approach for distinguishing potential contributions of pre-existing inhibitory control deficits vs.

Rodent models of attention-deficit hyperactivity disorder: An updated framework for model validation and therapeutic drug discovery.

There are over twenty rodent models of Attention-Deficit Hyperactivity Disorder (ADHD), with most reflecting a recognized ADHD subtype. Of these, only five rat models (Neonatal 6-Hydroxydopamine, Spontaneously Hypertensive Rat, Prenatal Alcohol Exposure, Prenatal Nicotine Exposure, and Lphn3 Knockout) and three mouse models (Dopamine Transporter Knockout, Neurokinin-1 Receptor Knockout, and Prenatal Nicotine Exposure) have a sufficient number of publications to explore their suitability for modelling ADHD with respect to core features, executive dysfunction, and medication effects. An updated view is advanced specifying that an informative model encompasses elevated drug use risk as a means to assess ADHD/Substance Use Disorder (SUD) comorbidity, a common co-occurrence among patients.