In the present study, we found that cocaine exposure stimulates m

In the present study, we found that cocaine exposure stimulates mTOR activity in rat brain. Furthermore, inhibition of mTOR by rapamycin blocked the induction as well as the expression of cocaine-induced locomotor sensitization in rats. These data elucidate a novel mechanism by which the mTOR pathway mediates cocaine-induced

behavioral changes and could suggest a new interventional strategy for drug abuse. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“During a settlement decision, the presence of conspecifics is crucial to species subject to Allee effects, for which the number of founders affects the subsequent growth of the colony. Marking the area (physically or chemically) conveys information about the number of GSK2118436 manufacturer conspecifics present in a new patch. Here, we study how an individual affinity for the marker affects the dynamics Elafibranor of a foundation process. A generic population model is presented, in which marking and affinity for the marker are at stake. Our results show that population size thresholds can appear, below which settlement is not possible. This model is then used to study the dynamics of migration and aggregation in a set of interconnected populations. We show that affinity for the marker can induce asymmetries

in the population distribution. Anelosimus eximius is a social spider subject to Allee effects, for which silk potentially acts as a marker. We test our predictions with field experiments involving two populations of A. eximius in a Y-shaped setup. The agreement between our experimental and theoretical results strongly supports the validity of the model. This allows us to use the model to estimate a realistic set of parameters of biological significance to this social spider. (C) 2010 Elsevier Ltd. All rights reserved.”
“The clinical course of the degenerative motor neuron disorder amyotrophic lateral sclerosis (ALS) is closely related to hypoxia. The normal response to hypoxia involves two pathways

in particular: the hypoxia inducible factor 1 alpha (HIF-1 alpha) pathway (which notably controls the synthesis of vascular endothelial growth factor (VEGF)) and the nuclear factor kappa B (NF-kappa b) pathway (responsible for the production of inflammatory mediators, including prostaglandin E2 (PGE(2))). Defects Cilengitide solubility dmso in VEGF gene expression are known to cause motor neuron degeneration in animal models. Circulating monocytes are precursors of the microglia, which are involved in the pathogenesis of ALS. To establish whether the HIF-1 and/or NF-kappa B pathways are deregulated during hypoxia in early-stage, sporadic ALS, we analyzed the response to acute (1 h) and prolonged (24 h) hypoxia in monocytes from ALS and healthy controls. We measured protein expression and mRNA transcription for VEGF, HIF-1, HIF-2, prolyl hydroxylases 1 and 2 (PHD-1 and -2, part of the HIF proteasome-dependent degradation pathway) and their modulation by PGE(2).

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