Chronic Drinking During Adolescence Predisposes the Adult Rat for Continued Heavy Drinking: Neurotrophin and Behavioral Adaptation after Long-Term, Continuous Ethanol Exposure

Previous research has found that adolescent ethanol (EtOH) exposure alters drug seeking behaviors, cognition and neuroplasticity. Using male Sprague Dawley rats, differences in spatial working memory, non-spatial discrimination learning and behavioral flexibility were explored as a function of age at the onset (mid-adolescent vs. adult) of chronic EtOH exposure (CET). Concentrations of mature brain-derived neurotrophic factor (mBDNF) and betanerve growth factor (beta-NGF) in the prefrontal cortex and hippocampus were also assessed at different time-points: during CET, following acute abstinence (48-hrs), and after protracted abstinence (6-8 wks). Our results revealed that an adolescent onset of CET leads to increased EtOH consumption that persisted into adulthood. In both adult and adolescent onset CET groups, there were significant long-term reductions in prefrontal cortical mBDNF and beta-NGF levels. However, only adult onset CET rats displayed decreased hippocampal BDNF levels. Spatial memory, assessed by spontaneous alternation and delayed alternation, was not significantly affected by CET as a function of age of drinking onset, but higher blood-EtOH levels were correlated with lower spontaneous alternation scores. Regardless of the age of onset, EtOH exposed rats were impaired on non-spatial discrimination learning and displayed inflexible behavioral patterns upon reversal learning. Our results indicate that adolescent EtOH exposure changes long-term consumption patterns producing behavioral and neural dysfunctions that persist across the lifespan

BB Potentials in Quenched Lattice QCD

The potentials between two B-mesons are computed in the heavy-quark limit using quenched lattice QCD at $m_\pi\sim 400~{\rm MeV}$. Non-zero central potentials are clearly evident in all four spin-isospin channels, (I,s_l) = (0,0) , (0,1) , (1,0) , (1,1), where s_l is the total spin of the light degrees of freedom. At short distance, we find repulsion in the $I\ne s_l$ channels and attraction in the I=s_l channels. Linear combinations of these potentials that have well-defined spin and isospin in the t-channel are found, in three of the four cases, to have substantially smaller uncertainties than the potentials defined with the s-channel (I,s_l), and allow quenching artifacts from single hairpin exchange to be isolated. The BB*\pi coupling extracted from the long-distance behavior of the finite-volume t-channel potential is found to be consistent with quenched calculations of the matrix element of the isovector axial-current. The tensor potentials in both of the s_l = 1 channels are found to be consistent with zero within calculational uncertainties.Comment: 30 page

Winning and losing: differences in reward and punishment sensitivity between smokers and nonsmokers

Background: Smokers show increased brain activation in reward processing regions in response to smoking-related cues, yet few studies have examined secondary rewards not associated with smoking (i.e., money). Inconsistencies exist in the studies that do examine secondary rewards with some studies showing increased brain activation in reward processing brain regions, while others show decreased activation or no difference in activation between smokers and nonsmokers. Aims: The goal of the current study is to see if smokers process the evaluation and delivery of equally salient real world rewards similarly or differently than nonsmokers. Methods: The current study employed functional magnetic resonance imaging (fMRI) to examine brain responses in smokers and nonsmokers during the evaluation and delivery of monetary gains and losses. Results: In comparison to nonsmokers, smokers showed increased activation in the ventromedial prefrontal cortex to the evaluation of anticipated monetary losses and the brain response. Moreover, smokers compared to nonsmokers showed decreased activation in the inferior frontal gyrus to the delivery of expected monetary gains. Brain activations to both the evaluation of anticipated monetary losses and the delivery of expected monetary gains correlated with increased self-reported smoking craving to relieve negative withdrawal symptoms and craving related to positive aspects of smoking, respectively. Discussion: Together these results indicate that smokers are hyperresponsive to the evaluation of anticipated punishment and hyporesponsive to the delivery of expected rewards. Although further research is needed, this hypersensitivity to punishments coupled with increased craving may negatively impact quit attempts as smokers anticipate the negative withdrawal symptoms associated with quitting

SU(2) Low-Energy Constants from Mixed-Action Lattice QCD

An analysis of the pion mass and pion decay constant is performed using mixed-action Lattice QCD calculations with domain-wall valence quarks on ensembles of rooted, staggered n_f = 2+1 MILC configurations. Calculations were performed at two lattice spacings of b~0.125 fm and b~0.09 fm, at two strange quark masses, multiple light quark masses, and a number of lattice volumes. The ratios of light quark to strange quark masses are in the range 0.1 <= m_l / m_s <= 0.6, while pion masses are in the range 235 < m_\pi < 680 MeV. A two-flavor chiral perturbation theory analysis of the Lattice QCD calculations constrains the Gasser-Leutwyler coefficients bar{l}_3 and bar{l}_4 to be bar{l}_3 = 4.04(40)(+73-55) and bar{l}_4 = 4.30(51)(+84-60). All systematic effects in the calculations are explored, including those from the finite lattice space-time volume, the finite lattice spacing, and the finite fifth dimension in the domain-wall quark action. A consistency is demonstrated between a chiral perturbation theory analysis at fixed lattice spacing combined with a leading order continuum extrapolation, and the mixed-action chiral perturbation theory analysis which explicitly includes the leading order discretization effects. Chiral corrections to the pion decay constant are found to give f_\pi / f = 1.062(26)(+42-40) where f is the decay constant in the chiral limit. The most recent scale setting by the MILC Collaboration yields a postdiction of f_\pi = 128.2(3.6)(+4.4-6.0)(+1.2-3.3) MeV at the physical pion mass.Comment: 28 pages, 9 figures; version 2 accepted for publication in PR

L’évolution et le développement du langage humain chez Homo Symbolicus et Pan Symbolicus

Bien que la dichotomie classique homme/animal continue de sous-tendre la pensée scientifique occidentale, la génétique moléculaire prouve que les humains sont bien plus proches des chimpanzés et des bonobos que ne pouvaient le supposer les chercheurs en se fondant seulement sur l’évidence anatomique, il y a quelques décennies. Le degré de similitude de l’ADN entre humains, bonobos et chimpanzés autorise à nous classer tous trois comme espèces-sœurs. Ce qui signifie, aussi étrange que cela pui..

Branding and a child’s brain: an fMRI study of neural responses to logos

Branding and advertising have a powerful effect on both familiarity and preference for products, yet no neuroimaging studies have examined neural response to logos in children. Food advertising is particularly pervasive and effective in manipulating choices in children. The purpose of this study was to examine how healthy children’s brains respond to common food and other logos. A pilot validation study was first conducted with 32 children to select the most culturally familiar logos, and to match food and non-food logos on valence and intensity. A new sample of 17 healthy weight children were then scanned using functional magnetic resonance imaging. Food logos compared to baseline were associated with increased activation in orbitofrontal cortex and inferior prefrontal cortex. Compared to non-food logos, food logos elicited increased activation in posterior cingulate cortex. Results confirmed that food logos activate some brain regions in children known to be associated with motivation. This marks the first study in children to examine brain responses to culturally familiar logos. Considering the pervasiveness of advertising, research should further investigate how children respond at the neural level to marketing

Importance of Reward and Prefrontal Circuitry in Hunger and Satiety: Prader-Willi Syndrome vs. Simple Obesity

Background: The majority of research on obesity has focused primarily on clinical features (eating behavior, adiposity measures), or peripheral appetite-regulatory peptides (leptin, ghrelin). However, recent functional neuroimaging studies have demonstrated that some reward circuitry regions which are associated with appetite-regulatory hormones are also involved in the development and maintenance of obesity. Prader-Willi syndrome (PWS), characterized by hyperphagia and hyperghrelinemia reflecting multi-system dysfunction in inhibitory and satiety mechanisms, serves as an extreme model of genetic obesity. Simple (non-PWS) obesity (OB) represents an obesity control state. Objective: This study investigated subcortical food motivation circuitry and prefrontal inhibitory circuitry functioning in response to food stimuli before and after eating in individuals with PWS compared with OB. We hypothesized that groups would differ in limbic regions (i.e., hypothalamus, amygdala) and prefrontal regions associated with cognitive control [i.e., dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC)] after eating. Design and Participants: Fourteen individuals with PWS, 14 BMI- and age-matched individuals with OB, and 15 age-matched healthy-weight controls (HWC) viewed food and non-food images while undergoing functional MRI before (pre-meal) and after (post-meal) eating. Using SPM8, group contrasts were tested for hypothesized regions: hypothalamus, nucleus accumbens (NAc), amygdala, hippocampus, OFC, medial PFC, and DLPFC. Results: Compared with OB and HWC, PWS demonstrated higher activity in reward/limbic regions (NAc, amygdala) and lower activity in hypothalamus and hippocampus, in response to food (vs. non-food) images pre-meal. Post-meal, PWS exhibited higher subcortical activation (hypothalamus, amygdala, hippocampus) compared to OB and HWC. OB showed significantly higher activity versus PWS and HWC in cortical regions (DLPFC, OFC) associated with inhibitory control. Conclusion: In PWS compared with obesity per se, results suggest hyperactivations in subcortical reward circuitry and hypoactivations in cortical inhibitory regions after eating, which provides evidence of neural substrates associated with variable abnormal food motivation phenotypes in PWS and simple obesity