Using Pop Culture to Teach Youths Conflict Resolution, Healthful Lifestyles, Disaster Preparedness, and More

Adolescents learn sustainable production techniques, civic engagement, leadership, public speaking, food safety practices, conflict resolution, disaster preparedness, and other life skills through Extension programming. Educators can increase participant interest in such programming by applying a creative pop culture twist, such as a zombie apocalypse theme. A pop culture take on a traditional topic infuses the educational experience with excitement and fun, which researchers stress increase motivation and learning. Who knew that understanding the U.S. government\u27s structure and recognizing the importance of voting could thwart development of a biological weapon that might spawn a zombie apocalypse? Creative thinking such as this can engage learners and increase registration numbers in youth development programs

Basolateral and central amygdala differentially recruit and maintain dorsolateral striatum-dependent cocaine-seeking habits.

In the development of addiction, drug seeking becomes habitual and controlled by drug-associated cues, and the neural locus of control over behaviour shifts from the ventral to the dorsolateral striatum. The neural mechanisms underlying this functional transition from recreational drug use to drug-seeking habits are unknown. Here we combined functional disconnections and electrophysiological recordings of the amygdalo-striatal networks in rats trained to seek cocaine to demonstrate that functional shifts within the striatum are driven by transitions from the basolateral (BLA) to the central (CeN) amygdala. Thus, while the recruitment of dorsolateral striatum dopamine-dependent control over cocaine seeking is triggered by the BLA, its long-term maintenance depends instead on the CeN. These data demonstrate that limbic cortical areas both tune the function of cognitive territories of the striatum and thereby underpin maladaptive cocaine-seeking habits.This work was supported by the Fondation pour la Recherche Médicale (FRM), the United Kingdom Medical Research Council (MRC) Grant 9536855 to BJE, the AXA research fund to ABR, an INSERM Avenir and an Agence Nationale de la Recherche (ANR) grant ANR12 SAMA00201 to DB. Research was conducted within both the MRC/Wellcome Trust Behavioral and Clinical Neuroscience Institute of Cambridge and the Inserm team “Psychobiology of Compulsive Disorders”, University of Poitiers.This is the final version of the article. It was first available from NPG via http://dx.doi.org/10.1038/ncomms1008

The effect of early psychostimulant treatment on abuse liability and dopamine receptors

Examines whether the reinforcing properties of drugs of abuse were altered in adulthood by methylphenidate, more commonly known as Ritalin. Subjects were 108 rats of Sprague-Dawley descent (Harlan). Methylphenidate, or saline was administered daily to the subjects from the postnatal period (11-20 days old). The rats preference for morphine during early adulthood was measured using conditioned place preference. The number of dopamine D₂ receptors was measured in each rat and the correlation between receptor number and morphine preference was determined. Results indicate that rats pretreated with methylphenidate showed greater preference for morphine than saline pretreated rats and suggests that exposure to methylphenidate during the postnatal period increases the rewarding value of morphine

Neurochemical substrates linked to impulsive and compulsive phenotypes in addiction: A preclinical perspective.

Funder: Institute for Neuroscience at Cambridge UniversityFunder: GlaxoSmithKline; Id: http://dx.doi.org/10.13039/100004330Funder: Boehringer Ingelheim Pharma GmbHDrug compulsion manifests in some but not all individuals and implicates multifaceted processes including failures in top-down cognitive control as drivers for the hazardous pursuit of drug use in some individuals. As a closely related construct, impulsivity encompasses rash or risky behaviour without foresight and underlies most forms of drug taking behaviour, including drug use during adverse emotional states (i.e., negative urgency). While impulsive behavioural dimensions emerge from drug-induced brain plasticity, burgeoning evidence suggests that impulsivity also predates the emergence of compulsive drug use. Although the neural substrates underlying the apparently causal relationship between trait impulsivity and drug compulsion are poorly understood, significant advances have come from the interrogation of defined limbic cortico-striatal circuits involved in motivated behaviour and response inhibition, together with chemical neuromodulatory influences from the ascending neurotransmitter systems. We review what is presently known about the neurochemical mediation of impulsivity, in its various forms, and ask whether commonalities exist in the neurochemistry of compulsive drug-motivated behaviours that might explain individual risk for addiction

Deterioro cognitivo en personas que consumen benzoilmetilecgonina y sus derivados. Una revisión bibliográfica

El consumo crónico o excesivo de la sustancia benzoilmetilecgonina y sus derivados se ha visto involucrado en el decremento del área cognitiva del ser humano, enfocándose en la: memoria, atención, concentración, orientación y diversas funciones cognitivas. El presente estudio trata de analizar los mecanismos subyacentes del deterioro cognitivo en personas adictas a la benzoilmetilecgonina y denotar los instrumentos métricos presentados en esta línea de estudio. Mediante una revisión sistemática en las bases de datos Pub Med y Medline, se lograron discriminar 51 artículos científicos no aleatorizados relacionados con la temática. Los artículos fueron analizados mediante la herramienta AMSTAR y descritos con la metodología PRIMA. Como resultado del análisis, se concluyó que el deterioro cognitivo es evidente y progresivo en sus funciones cognitivas de pacientes evaluados. La actualización de esta información permitirá aportar a futuras investigaciones e intervenciones sobre la concientización del consumo.Chronic or excessive consumption of the substance benzoylmethylecgonine and its derivatives has been involved in the decrease in the cognitive area of the human being, focusing on: memory, attention, concentration, orientation and various cognitive functions. The present study tries to analyze the underlying mechanisms of cognitive deterioration in people addicted to benzoylmethylecgonine and denote the metric instruments presented in this line of study. Through a systematic review in the Pub Med and Medline databases, it was possible to discriminate 51 non-randomized scientific articles related to the subject. The articles were analyzed using the AMSTAR tool and described with the PRIMA methodology. As a result of the analysis, it was concluded that cognitive impairment is evident and progressive in their cognitive functions in evaluated patients. Updating this information will make it possible to contribute to future research and interventions on consumer awareness

Amino acids contribute to adaptive thermogenesis. New insights into the mechanisms of action of recent drugs for metabolic disorders are emerging

Adaptive thermogenesis is the heat production by muscle contractions (shivering thermogenesis) or brown adipose tissue (BAT) and beige fat (non-shivering thermogenesis) in response to external stimuli, including cold exposure. BAT and beige fat communicate with peripheral organs and the brain through a variegate secretory and absorption processes − controlling adipokines, microRNAs, extracellular vesicles, and metabolites − and have received much attention as potential therapeutic targets for managing obesity-related disorders. The sympathetic nervous system and norepinephrine-releasing adipose tissue macrophages (ATM) activate uncoupling protein 1 (UCP1), expressed explicitly in brown and beige adipocytes, dissolving the electrochemical gradient and uncoupling tricarboxylic acid cycle and the electron transport chain from ATP production. Mounting evidence has attracted attention to the multiple effects of dietary and endogenously synthesised amino acids in BAT thermogenesis and metabolic phenotype in animals and humans. However, the mechanisms implicated in these processes have yet to be conclusively characterized. In the present review article, we aim to define the principal investigation areas in this context, including intestinal microbiota constitution, adipose autophagy modulation, and secretome and metabolic fluxes control, which lead to increased brown/beige thermogenesis. Finally, also based on our recent epicardial adipose tissue results, we summarise the evidence supporting the notion that the new dual and triple agonists of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon (GCG) receptor − with never before seen weight loss and insulin-sensitizing efficacy − promote thermogenic-like amino acid profiles in BAT with robust heat production and likely trigger sympathetic activation and adaptive thermogenesis by controlling amino acid metabolism and ATM expansion in BAT and beige fat

Reductions in Mesolimbic Dopamine Signaling and Aversion: Implications for Relapse and Learned Avoidance

The ability to adjust behavior appropriately following an aversive experience is essential for survival, yet variability in this process contributes to a wide range of disorders, including drug addiction. It is clear that proper approach and avoidance is regulated, in part, by the activity of the mesolimbic dopamine system. While the importance of this system as a critical modulator of reward learning has been extensively characterized, its involvement in directing aversion-related behaviors and learning is still poorly understood. Recent studies have revealed that aversive stimuli and their predictors cause rapid reductions in nucleus accumbens (NAc) dopamine concentrations. Furthermore, a normally appetitive stimulus that is made aversive through association with cocaine also decreases dopamine, and the magnitude of the expressed aversion predicts drug-taking. However, whether the presentation of a drug cue that reduces dopamine, and evokes a negative affective state, can motivate relapse is unknown. Here we demonstrate that the presentation of an aversive drug cue both reduces dopamine and causes cocaine-seeking. This finding is provocative because drug seeking in reinstatement designs is typically associated with increased dopamine signaling. Using a combination of fast scan cyclic voltammetry (FSCV) and in vivo electrophysiology we subsequently show that the presence of an aversive drug cue abolishes the dopaminergic encoding of other drug cues and alters NAc neuronal activity patterns. Importantly, a subpopulation of neurons that subsequently encode aspects of drug-seeking behavior increase their baseline firing rates during this aversive experience. We then examine the mechanistic regulation of dopamine signaling by aversive stimuli under more natural conditions. Using FSCV and site-specific behavioral pharmacology we demonstrate that blockade of ventral tegmental area kappa opioid receptors attenuates aversion-induced reductions in dopamine, and prevents proper avoidance learning caused by punishment. By maintaining D2 receptor occupancy within the NAc during punishment, we demonstrate the requirement of aversion-induced reductions in dopamine for aversive learning. Together, these studies inform an evolving model of striatal physiology. Our findings emphasize a role for both increases and decreases in dopamine signaling that modulate behavior by promoting the stimulus-specific activity of distinct striatal output pathways. The continued interrogation of this model may offer novel targets for therapeutic development aimed at treating neurodegenerative disease and drug addiction

COCAINE-INDUCED BEHAVIORAL SENSITIZATION AND CONDITIONED PLACE PREFERENCE IN JAPANESE QUAIL (\u3cem\u3eCOTURNIX JAPONICA\u3c/em\u3e): A FOCUS ON SEX DIFFERENCES AND DOPAMINERGIC MECHANISMS

Research has indicated that gonadal hormones may mediate behavioral and biological responses to cocaine. Estrogen, in particular, has been shown to increase behavioral responding to cocaine in female rats relative to male rats. The use of Japanese quail may add to our knowledge of sex differences in drug abuse because of their advanced visual system and the ability to control their gonadal hormones via alterations in photoperiod. In three experiments, cocaine-induced behaviors were examined using this avian model. In Experiment 1, I investigated the potential sex differences in cocaine-induced locomotor activity between male and female Japanese quail and I examined the potential role of gonadal hormones in these effects. Results from Experiment 1 indicated that cocaine-induced locomotor activity correlates with testosterone in male quail. Surprisingly, cocaine-induced activity did not correlate with estradiol in female quail, nor did female quail respond to cocaine as expected. Due to these results, Experiment 2 was designed to determine whether D2 receptors are involved in the psychomotor activating effects of cocaine in female quail. Results from Experiment 2 showed that D2 blockade enhances acute cocaine-induced locomotor activity in female quail. This result suggests that D2 receptors play an important role in cocaine-induced locomotor activity in female quail. Cocaine’s psychomotor and rewarding properties are typically attributed to different neural mechanisms and are thought to represent different aspects of drug abuse. In Experiment 3, the rewarding properties of cocaine were examined in female quail using a CPP procedure. Additionally, Experiment 3 examined the potential role of estradiol in those effects. Results from Experiment 3 revealed that cocaine is dose-dependently rewarding and estradiol may enhance the rewarding properties of cocaine in female quail. Taken together, the present work suggests that gonadal hormones may play an important role in both the psychomotor activating effects and rewarding properties of cocaine in Japanese quail. Additionally, the collective results add to our understanding of the underlying hormonal and neurobiological mechanisms that may mediate sex differences in cocaine-induced behaviors

Addictive behaviour in experimental animals: prospects for translation.

Since the introduction of intravenous drug self-administration methodology over 50 years ago, experimental investigation of addictive behaviour has delivered an enormous body of data on the neural, psychological and molecular mechanisms of drug reward and reinforcement and the neuroadaptations to chronic use. Whether or not these behavioural and molecular studies are viewed as modelling the underpinnings of addiction in humans, the discussion presented here highlights two areas-the impact of drug-associated conditioned stimuli-or drug cues-on drug seeking and relapse, and compulsive cocaine seeking. The degree to which these findings translate to the clinical state of addiction is considered in terms of the underlying neural circuitry and also the ways in which this understanding has helped develop new treatments for addiction. The psychological and neural mechanisms underlying drug memory reconsolidation and extinction established in animal experiments show particular promise in delivering new treatments for relapse prevention to the clinic.This article is part of a discussion meeting issue 'Of mice and mental health: facilitating dialogue between basic and clinical neuroscientists'