These results seem to support the claims made by the kinematic theory that a motor command is emitted at time t0, the time reference parameter of the model. This article proposes a new time marker directly associated with a cerebral event (i.e. the emission of a motor command) that can be used for the development of new data analysis methodologies and for Panobinostat clinical trial the elaboration of new experimental

protocols based on ERP. “
“Despite the widespread use of mice as models of Parkinson’s disease there is a surprising lack of validation and characterisation of unilateral lesion models in mice and the extent of behavioural impairments induced by such lesions. The aim of the present study was to characterise the behavioural deficits observed after injection selleck compound of

6-hydroxydopamine unilaterally into the substantia nigra, and correlate the behavioural impairments with the extent of damage to the mesostriatal dopaminergic pathway. We found that a recently introduced test for assessment of sensorimotor impairment, the corridor task, was particularly useful in determining lesion severity, and that this test, in combination with standard drug-induced rotation tests, can be used to select animals with profound (≥ 80%) dopaminergic lesions that are stable over time. Based on these data we propose criteria that can be used to predict the extent of lesion, classified as severe, intermediate or mild lesions of the mesostriatal pathway. The correlation of cell loss and striatal innervation

with the performance in each test provides a useful tool for the assessment of functional recovery in neurorestoration and cell transplantation studies, and for the evaluation Resminostat of the in vivo efficacy and performance of stem cell-derived dopamine neuron preparations. Damage to the midbrain dopamine (DA) neurons induced by systemic injections of 1-methyl-1,2,3,4-tetrahydropyridine (MPTP) is the most commonly used model of Parkinson’s disease (PD) in mice. The MPTP model is highly valuable as a model of neurotoxin-induced oxidative and mitochondrial damage, and is particularly attractive as it avoids the use of more specialised stereotaxic surgery. However, the MPTP model is less useful for functional studies as the lesion-induced behavioural impairments are quite subtle and also strain-dependent (Sedelis et al., 2000), and unless a very heavy treatment regimen is used (e.g., 10 injections of 25 mg/kg + probenecid over 5 weeks; Meredith et al., 2008) the impairments are mostly transient (Sedelis et al., 2001). The bilateral deficits seen in MPTP-treated mice are also more difficult to quantify and distinguish from more general sickness-related behaviour.