The Porsolt swim test usually

involves two swim exposures separated by 24 h, and we asked whether the 2-AG response differed between the first and second exposures. Methods: Four groups of male C57/BI6N mice were studied: control; exposed to a single 6 min swim and killed immediately; exposed to a single 6 min swim and killed 24 h later; and exposed to two swims, SP600125 purchase separated by 24 h, and killed after the second swim. Outcomes were swim behavior, serum corticosterone, and 2-AG and 2-oleoylglycerol (2-OG) contents in amygdala, hippocampus, and prefrontal cortex. Results: Mean 2-AG contents were not significantly different among the four treatment groups in any brain region and did not correlate with immobility in either forced swim exposure. However, 2-AG contents in all three brain regions only of the mice exposed to two swims were significantly, positively correlated with serum corticosterone concentrations measured at the same time. 2-OG is present in brain and exhibits a striking regional heterogeneity in control mice. 2-OG concentrations in prefrontal cortex were significantly reduced in the mice killed on the second day compared with the mice killed on the first day. As the target

of 2-OG in brain is not known, the significance of these observations await further selleckchem studies. Conclusions: Although prior exposure to swim stress does not alter brain 2-AG contents upon re-exposure, 2-AG concentrations in brain become significantly correlated

with the hypothalamic-pituitary-adrenal (HPA) axis response to stress when prior exposure to the stress has occurred. These data suggest that even a single exposure to a short period of intense stress sensitizes the 2-AG response to re-exposure to that situation and are consistent with a role for endocannabinoid signaling in modulating stress responses.

This article is part of a Special Issue entitled: Stress, Emotional Behavior and the Endocannabinoid System. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The past few Volasertib supplier years have seen significant advances in the identification of genetic factors that contribute to complex disease. Progress in cardiovascular diseases (CVD) has been particularly impressive, with genome-wide association studies (GWAS) leading to the identification of similar to 160 loci associated with CVD and its risk factors, many of which implicate new biological pathways. Here we focus on our growing understanding of the genetic contribution to CVD, examining the gene variants that increase the risk of particular CVD events and those underlying traditional CVD risk factors. Although GWAS face several technical challenges, including the potential for both false-positive and false-negative findings, they are starting to provide a unique view of the genetic architecture of a common disease.