Topic: motor impairments

In our previous studies, we developed a marker-based 3D motion capture system to evaluate step kinematics during behaviors such as climbing and novel environment exploration under various pharmacological treatments. In the present study, we aimed to test whether the step kinematics of mice is affected during treadmill running at different speeds and under various treatments. We used adult male C57BL/6 mice in a within-subject, randomized design. We recorded voluntary running behavior on a treadmill in mice treated with vehicle (1:1:18 ethanol, Kolliphor, saline), CP55,940 (0.3 mg/kg) or harmal

Brain L-serine is critical for neurodevelopment and is thought to be synthesized solely from glucose. In contrast, we found that the influx of L-serine across the blood–brain barrier (BBB) is essential for brain development. We identified the endothelial Slc38a5, previously thought to be a glutamine transporter, as an L-serine transporter expressed at the BBB in early postnatal life. Young Slc38a5 knockout (KO) mice exhibit developmental alterations and a decrease in brain L-serine and D-serine, without changes in serum or liver amino acids. Slc38a5-KO brains exhibit accumulation of neurotoxic

Aim: The intricate development of Parkinson's disease (PD) has posed a significant challenge in finding effective treatments. In the current study, a diaryl pyrrole compound, 1-(2-chlorophenyl)-2-methyl-5-(4-chlorophenyl)-1H-Pyrrole, was designed, synthesized, and tested for possible motor function improvement in 6-hydroxydopamine (6-OHDA) induced neurotoxicity in a rat model of PD.Method: Parkinsonism was triggered unilaterally by injecting 6-OHDA (12μg/4μl/rat) into the striatum. The compound (1,5,10 and 30 mg/kg) was then given intraperitoneally for 14 consecutive days following the 6-OHDA

Amyotrophic lateral sclerosis (ALS) is a fatal and non-curable neurodegenerative disease for which the etiology remains poorly understood. However, among the pathophysiological hallmarks observed both in patients and in animal models, mitochondrial dysfunctions appear to be one of the earliest events and thus might be causative for the progressive loss of motor neurons (Le Masson et al, 2014). Therefore, restoring mitochondrial functions could be a therapeutic area of interest in the development of new therapies in the context of ALS.For this purpose, we are interested in the Bornavirus X prot