Response rate decreasing effects of naloxone during chronic sucrose availability.

Studies in animal models suggest that sugar deprivation following excessive intake elicits some opioid-like withdrawal signs. In the present study, opioid-like effects of excessive sucrose intake were further characterized in C57BL/6 mice by comparing the effects of the opioid antagonist naloxone on food-reinforced responding before and during sucrose availability and, in parallel experiments, following chronic morphine administration. Results show that naloxone produced time-dependent and dose-dependent decreases in operant response rates after 4 weeks of excessive sucrose consumption, and that these effects were comparable with those produced by chronic morphine injections. These findings extend the observation that excessive sucrose consumption may produce opioid-like withdrawal signs, and suggest that operant assays of withdrawal-suppressed behaviors may be useful for further study of excessive sucrose consumption.

Food and addiction among the ageing population.

Obesity among the elderly is a growing public health concern. Among the various factors that may contribute to the current rates of obesity is the rewarding aspect of highly palatable foods and beverages, which may lead to overconsumption and excess caloric intake. The present review describes recent research supporting the hypothesis that, for some individuals, the consumption these highly palatable foods and beverages may lead to the development of addictive-like behaviors. In particular, the authors consider the relevance of this hypothesis to the ageing population.

Receptor dimerization dynamics as a regulatory valve for plasticity of type I interferon signaling.

Type I interferons (IFNs) activate differential cellular responses through a shared cell surface receptor composed of the two subunits, IFNAR1 and IFNAR2. We propose here a mechanistic model for how IFN receptor plasticity is regulated on the level of receptor dimerization. Quantitative single-molecule imaging of receptor assembly in the plasma membrane of living cells clearly identified IFN-induced dimerization of IFNAR1 and IFNAR2. The negative feedback regulator ubiquitin-specific protease 18 (USP18) potently interferes with the recruitment of IFNAR1 into the ternary complex, probably by impeding complex stabilization related to the associated Janus kinases. Thus, the responsiveness to IFNα2 is potently down-regulated after the first wave of gene induction, while IFNß, due to its ∼100-fold higher binding affinity, is still able to efficiently recruit IFNAR1. Consistent with functional data, this novel regulatory mechanism at the level of receptor assembly explains how signaling by IFNß is maintained over longer times compared with IFNα2 as a temporally encoded cause of functional receptor plasticity.

Further developments in the neurobiology of food and addiction: update on the state of the science.

Over the past three decades, obesity has become a major public health crisis in the United States. The prevalence of obesity in the United States and in other parts of the world has led to a new word, "globesity," being used to describe the problem. As a result of this increased emphasis on understanding the causes and consequences of obesity, novel theories have stimulated new research aimed to prevent, intervene in and ameliorate the effects and decrease the incidence and medical consequences of globesity. One theory that has gained popularity in recent years, is based on the idea that an excessive intake of highly palatable foods shares similarities with the effects on brain and behavior that are seen with some drugs of abuse. Although this theory is not new, empirically-based translational research has only recently provided strong support for this hypothesis. In the present article, we review the present state of the science in this area and describe some newer clinical and preclinical works that shed light on innovative and interesting overlaps between excessivly palatable food intake and drug use.