Given the difficulties of replicating lifelong calorie restriction within human populations, we have sought to assess the effects of short-term adult-onset calorie restriction upon acute excitotoxic insults in the rat hippocampus. Adult animals (approximately 6 months of age) underwent calorie restriction (alternate day feeding) for 7-10 weeks. Utilizing both electrophysiological and immunocytochemical techniques, we report that calorie restriction had no effect upon long-term

potentiation (LTP), a measure of neuronal function. In control animals, application of kainic acid JPH203 datasheet (20 mu M) resulted in only 35% recovery of CA1 population spikes post-insult. However calorie-restricted animals showed significantly improved recovery after kainic acid treatment (64%). This data was supported by immunocytochemical studies which noted widespread loss of microtubule-associated protein (MAP 2)

immunoreactivity in control slices following treatment with kainic acid; however MAP 2 staining was preserved in the CA1 and CA3 regions of calorie-restricted animals. Interestingly there was no significant difference in the recovery of population spikes between groups when slices were treated with N-methyl-D-aspartate (15 mu M). We conclude that short-term adult-onset calorie restriction does not alter normal neuronal function and serves to protect the hippocampus from acute kainic acid excitotoxicity. (c) 2007 Elsevier Ireland Ltd. All rights reserved.”
“Traumatic brain injury is accompanied by glial cell activation around the site of the injury. In this 17DMAG mw study, we investigated the role of toll-like receptor 2 (TLR2) in glial cell activation using a stab-wound injury (SWI) model with TLR2 knock-out mice. Penetration of a normal mouse brain with a 26-G needle using a stereotaxic instrument Etoposide in vitro resulted in an 18- and 4-fold upregulation

of GFAP and CD11b mRNA, respectively, along the needle track in the injury area. However, in the TLR2 knock-out mice, the induced expression of these genes was reduced by 70% and 40%, respectively. Likewise, there was a reduction in the area of activated glial cells detected by immunohistochemistry and the glial cells had a less-activated morphology in the TLR2 knock-out mice. In addition, the expression of the heme oxygenase-1 (HO-1) gene, a glia-expressing wound-responsive gene, was reduced after SWI in TLR2 knock-out mice. Taken together, these data argue that TLR2 contributes to the glial cell activation and HO-1 gene expression associated with traumatic brain injury. (c) 2007 Elsevier Ireland Ltd. All rights reserved.”
“Rather than attempt to provide a comprehensive account of air quality risk assessment, as might be found in a textbook or manual, this article discusses some issues that are of current importance in the United Kingdom and the rest of Europe, with special emphasis on risk assessment in the context of policy formulation, and emerging scientific knowledge.