Gait analyses showed that these walking velocity

adjustments result from simultaneous adaptations in both step length and step duration. The role of visual information in the control of self-motion velocity is discussed in relation with other factors. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Neurocognitive deficits seen in HIV-associated neurocognitive disorders (HANDs) are attributed to the release of soluble factors from CNS-resident, HIV-infected and/or activated macrophages and microglia. To study HIV-associated neurotoxicity, we used our in vitro model in which primary rat neuronal/glial cultures are treated with supernatants from cultured human monocyte-derived macrophages,

AZD0156 infected with a CNS-isolated HIV-1 strain (HIV-MDM). We found that neuronal damage, detected as a loss of microtubule-associated protein-2 (MAP2), begins as early as 2 hand is preceded by a loss of mitochondrial membrane potential (Delta psi(m)). Interestingly, inhibitors of calpains, but not inhibitors of caspases, blocked MAP2 loss, however neither selleck chemical type of inhibitor prevented the loss of Delta psi(m). To facilitate throughput for these studies, we refined a MAP2 cell-based-ELISA whose data closely compare with our standardized method of hand counting neurons. In addition, we developed a tetramethyl rhodamine methyl ester (TMRM)-based multi-well fluorescent plate assay for the evaluation of whole culture Delta psi(m). Together, these findings indicate that calpain activation and loss of Delta psi(m) may be parallel pathways to death in HIV-MDM-treated neurons and also demonstrate the validity of plate assays for assessing multiple experimental parameters as is useful for screening neurotherapeutics for neuronal damage and death. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Flucloronide Society. All rights reserved.”
“We examined whether chronic systemic

treatment with agonists for peroxisome proliferator-activated receptor alpha (PPAR alpha) influences neuroinflammation induced by lipopolysaccharide (LPS) injection into the somatosensory cortex in adult mice. Mice were pretreated with Wy-14643 or fenofibrate, both at 30 mg/kg, for 7 days. These treatment protocols increased the amount of PPAR alpha mRNA and active form of PPAR alpha protein in the brain. LPS injection reduced the PPAR alpha mRNA level in the brain. On the contrary, TNF alpha, IL-1 beta, IL-6, iNOS, COX-2, ICAM-1, VCAM-1, and PECAM-1 were elevated at 6 h after LPS. Wy-14643 and fenofibrate inhibited the elevations of TNF alpha, IL-1 beta, IL-6, COX-2, ICAM-1, and VCAM-1. Wy-14643, but not fenofibrate, also attenuated the iNOS elevation.