Stimulation of kappa-opioid receptors can increase ethanol intake, at least in long-term ethanol-experienced rats. Since kappa-opioid receptor agonists have aversive motivational consequences, increased ethanol drinking might be an attempt to counteract the aversive effects of this treatment. On the other hand, the nor-BNI experiments indicate that endogenous kappa-opioid receptor stimulation does not seem to be involved in relapse-like drinking after protracted abstinence.

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Emotionality is thought to be multidimensional, with "anxiety" representing one dimension. Dissecting emotional dimensions in animal models is an essential prerequisite for investigating the neurobiological mechanisms that underlie anxiety. The authors used factor analysis to investigate emotional dimensions in normal rats and rats bred for either high or low anxiety-related behavior. Hyperanxious rats were reduced in emotional dimensions in the elevated plus-maze by selection pressure, and a modified hole board test revealed a dissection of their emotionality with precisely defined dimensions. This enabled clear differentiation of "anxiety" from other emotional dimensions including risk assessment behavior and exploration. Factors extracted by analyzing data from a multiple-test battery corresponded to particular test characteristics rather than to emotional dimensions. The approach used might help to develop specific treatment strategies for anxiety disorders.

BackgroundIn a substantial proportion of depressed patients, stressful life events play a role in triggering the evolution of the illness. Exposure to stress has effects on different levels in laboratory animals as well and for the rat it has been shown that chronic mild stress (CMS) can cause antidepressant-reversible depressive-like effects. The adoption of the model to the mouse seems to be problematic, depending on the strain used and behavioural endpoint defined. Our aim was to evaluate the applicability of CMS to mice in order to induce behavioural alterations suggested to reflect depression-like symptoms.Methodology/Principal FindingsA weekly CMS protocol was applied to male mice of different mouse strains (D2Ola, BL/6J and BL/6N) and its impact on stress-sensitive behavioural measures (anhedonia-, anxiety- and depression-related parameters) and body weight was assessed. Overnight illumination as commonly used stressor in CMS protocols was particularly investigated in terms of its effect on general activity and subsequently derived saccharin intake. CMS application yielded strain-dependent behavioural and physiological responses including ‘paradox’ anxiolytic-like effects. Overnight illumination was found to be sufficient to mimic anhedonic-like behaviour in BL/6J mice when being applied as sole stressor.Conclusions/SignificanceThe CMS procedure induced some behavioural changes that are compatible with the common expectations, i.e. ‘anhedonic’ behaviour, but in parallel behavioural alterations were observed which would be described as ‘anomalous’ (e.g. decreased anxiety). The results suggest that a shift in the pattern of circadian activity has a particular high impact on the anhedonic profile. Changes in activity in response to novelty seem to drive the ‘anomalous’ behavioural alterations as well.

Introduction Monoamine-based antidepressants inhibit neurotransmitter reuptake within short time. However, it commonly takes several weeks until clinical symptoms start to resolve-indicating the involvement of effects distant from reuptake inhibition. Objective To unravel other mechanisms involved in drug action, a "reverse" pharmacological approach was applied to determine antidepressant-induced alterations of hippocampal gene expression. Materials and methodsThe behavioral response to longterm paroxetine administration of male DBA/2Ola mice was assessed by the forced swim test (FST), the modified hole board (mHB), and the dark/light box. Hippocampi of test-naive mice were dissected, and changes in gene expression by paroxetine treatment were investigated by means of microarray technology. Results and discussion Robust effects of paroxetine on passive stress-coping behavior in the FST were observed. Furthermore, anxiolytic properties of long-term antidepressant treatment could be identified in DBA mice in both, the mHB and dark/light box. Analysis of microarray results revealed a list of 60 genes differentially regulated by chronic paroxetine treatment. Preproenkephalin 1 and inhibin beta-A showed the highest level of transcriptional change. Furthermore, a number of candidates involved in neuroplasticity/neurogenesis emerged (e.g., Bdnf, Gfap, Vim, Sox11, Egr1, Stat3). Seven selected candidates were confirmed by in situ hybridization. Additional immunofluorescence colocalization studies of GFAP and vimentin showed more positive cells to be detected in long-term paroxetine-treated DBA mice. Conclusion Candidate genes identified in the current study using a mouse strain validated for its responsiveness to long-term paroxetine treatment add, in our opinion, to unraveling the mechanism of action of paroxetine as a representative for SSRIs.

According to the tension reduction hypothesis, individualsThe anxiolytic effect of alcohol may be one important motivation for its consumption, at least in individuals who are susceptible to this effect (Pohorecky 1981;Spanagel et al. 1995). It has been argued in the so-called "tension reduction hypothesis" by Conger (1956), that in situations where alcohol consumption is fear-reducing, this effect reinforces alcohol consumption and may, therefore, promote future alcohol intake. This hypothesis predicts that more anxious individuals should benefit more from the anxiolytic effect of alcohol and therefore consume more alcohol than less anxious individuals.The validity of this concept is still a matter of debate, because its direct assessment is difficult, and only a few

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The concept of stress-relief by alcohol has led to many investigations in order to elucidate the mechanisms of interactions of stress and alcohol, and the stress-reducing effect of alcohol as a motivation for alcohol consumption. The hypothalamo-pituitary-adrenocortical (HPA) system is one of the biological systems affected by both stress and alcohol. However, there is a high individual variation in the response of the HPA axis to either stress or alcohol. Factors like quality, severity and duration of stress, dose of alcohol and frequency of stress or alcohol exposure add to the individual response to stress or alcohol. The individual response is determined by interactions of genetic, environmental and experiential factors. Facing that complexity, with even more factors to be named, the often reported inconsistencies in both human and animal studies are not only attributable to methodological differences. Nevertheless, there are studies showing an influence of stress on alcohol consumption which most likely depends on the sample of probands examined. To our view, the concept of stress-relief by alcohol as a basic motivation for developing alcohol drinking habits is only applicable to subgroups of drinkers. Individuals with a dysfunctional HPA axis, inherited and/or acquired, might represent such a subgroup of stress-motivated drinkers.