Pregnant female Sprague-Dawley rats were treated with IBP via a subcutaneous Silastic capsule. Consequently, the offspring were exposed to IBP during gestation through the placentae, Selleckchem BMN673 and before weaning through the milk. Male and female offspring were tested for emotional behavior in an open field and in an elevated plus maze at five and six weeks old, respectively. IBP-exposed male (but not female) rats spent less time in the open arms of

the elevated plus maze. At 11 weeks old, all females were gonadectomized and treated chronically with 17 beta-estradiol or cholesterol by Silastic capsules; all males were kept intact. They were tested for learning performance in a passive avoidance test and a Morris water maze. IBP exposure impaired the performance of males in the passive avoidance test. These findings suggest that male rats are more affected by early exposure to IBP than female rats. IBP affects their adult behavior including anxiety and learning abilities. (C) 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights this website reserved.”
“Excretory-secretory products (ESP) from helminthic parasites may play pivotal roles in the immune regulation in hosts. Previously, we reported that ESP produced from Paragonimus westermani induced morphological activation of microglial cells and markedly stimulated nitric oxide (NO) production via activation of mitogen-activated

dipyridamole protein kinases (MAPKs). In the present study, we investigated

the role of protein kinase C and protein kinase A in MAPKs-dependent NO production by ESP. We found that treatment with protein kinase C inhibitor Go6976 strongly inhibited the phosphorylation of p38 and JNK, but not ERK, of MAPKs and decreased the production of NO in ESP-stimulated microglial cells. Inhibition of ERK, p38 or PKC decreased the ESP-induced activation of NF-kappa B, an important transcription factor for iNOS expression. Furthermore, ESP increased the level of p-CREB in microglial cells. However, adenylyl cyclase activator (forskolin). adenylyl cyclase inhibitor (SQ22536), cAMP analogue (db-cAMP) or protein kinase A inhibitor (H89) was not able to change iNOS expression and NO production in ESP-treated microglial cells. It implies that the cAMP-PKA-CREB pathway is not implicated in the ESP-evoked NO production in microglial cells. Thus, our results indicate that ESP stimulates microglial expression of iNOS via both PKC-dependent and -independent MAPKs phosphorylation and NF-kappa B activation. (C) 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Novel approaches are required in peripheral nerve injury management because current surgical techniques, which do not address axotomy-induced neuronal death, lead to deficient sensory recovery. Sensory neuronal death has functional preference with cutaneous neurons dying in great numbers whilst muscle afferents survive axotomy.