This REM sleep-specific change, in the absence of profound changes in wake motor behaviors, suggests that the MPTP marmoset model of PD could be used for further studies into the mechanisms and treatment of RBD and other sleep disorders in premotor symptom PD.

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Careful design of experiments using living organisms (e.g. mice) is of critical importance from both an ethical and a scientific standpoint. Randomization should, whenever possible, be an integral part of such experimental design to reduce bias thereby increasing its reliability and reproducibility. To keep the sample size as low as possible, one might take randomization one step further by controlling for baseline variations in the dependent variable(s) and/or certain known covariates. To give an example, in animal experiments aimed to study atherosclerosis development, one would want to control for baseline characteristics such as plasma triglyceride and total cholesterol levels and body weight. This can be done by first defining blocks to create balance among groups in terms of group size and baseline characteristics, followed by random assignment of the blocks to the various control and intervention groups. In the current study we developed a novel, user-friendly tool that allows users to easily randomize animals into blocks and identify random block divisions that are well-balanced based on given baseline characteristics, making randomization time-efficient and easy-to-use. Here, we present the resulting software tool that we have named RandoMice.

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Shock-induced behavioural sensitization in rats is reduced by acute treatment with a group II metabotropic glutamate receptor agonist. This effect may depend on the increased expression of amygdala mGluR3, which could be hypothesized as an endogenous mechanism to counteract stress-induced neuronal sensitization.

2.1 Etiology of Parkinson's disease Although Parkinson's disease has been studied for almost 200 years, the precise mechanisms leading to progressive cell death still need to be resolved; the actual cause and the mechanism(s) associated with the pathogenesis of Parkinson's disease are still unknown. However, it has been proposed that several factors including oxidative stress, excitotoxicity, mitochondrial dysfunction, environmental toxins, proteasome dysfunction, inflammatory aspects and genetic defects may contribute to the neurodegenerative process causing Parkinson's disease. Whatever the cause is, it is clear that Parkinson's disease is a multi-factorial disorder resulting from the combined effect of age, environmental factors, genetic susceptibility and complex genetic-environmental interactions (Fig. 1) (

The collagen antibody-induced arthritis (CAIA) model is highly effective in inducing arthritis, making it an attractive model for screening therapeutic compounds such as glucocorticoids (GCs). The severity of discomfort in this model makes it desirable to administer analgesics, but it is a prerequisite that these do not interfere with the model or tested therapeutics. In the present study, we studied the effect of 1 mg/mL tramadol and 3.5 mg/mL paracetamol (TP) on CAIA in male BALB/cAnNCrl mice and the possible interference of TP analgesia with the activity of the GC drug prednisolone (Pred). Our results showed that TP abolished the Pred-induced amelioration of CAIA, as well as several other Pred-induced effects, such as the reduction in thymus weight and the increase in insulin level. This most likely results from the effects of TP on the hepatic metabolism of this drug, since it strongly increased the Cyp3a11 expression in the liver. Altogether, we conclude that TP analgesia is not suitable for the CAIA model in male BALB/cAnNCrl mice, in particular when evaluating the effects of GCs such as Pred.