Small GTPases such as Rac1, are believed to be critical regulators of these processes. We have previously reported that Rac1 is highly expressed in mouse hippocampus, where NMDA receptor activation causes Rac1 to translocate to the membrane in a manner similar to that observed in other non-neuronal cells. Additionally selleck Rac1 has been seen to play a role in activation of signal transduction pathways associated with hippocampal learning and memory. Because of the established role of LTP and LTD in learning and memory processes, in this study we investigate whether Rac1 plays also an active and critical role in these

types of long-term synaptic plasticity. We found that activation of Rac1 is associated with long-term plasticity, both LTP and LTD. Rac1 appears to have a transient role during the induction of NMDA receptor-dependent LTP, but does not have an effect on LIP maintenance and expression. Similar results were found for NMDA receptor-dependent induction of LTD, while mGluR-dependent LTD was shown to be significantly altered YM155 molecular weight but not abolished. The

results of these experiments provide essential knowledge regarding the signaling mechanisms that underlie synaptic plasticity, as well as learning and memory processes, which in turn offers insights into the basis of diseases involving memory impairment, such as Fragile X syndrome, Alzheimer’s disease, William’s syndrome, Angelman syndrome (AS), and schizophrenia. (C) 2011 Elsevier Ltd. All rights reserved.”
“Bacillus subtilis has been engineered successfully to express heterologous antigens for use as a vaccine vehicle that can elicit mucosal and systemic immunity response. In this study, a recombinant B. subtilis expressing the B subunit of cholera toxin (CT-B) and an epitope box constituted with antigen sites from foot-and-mouth disease virus (FMDV) type Asia 1 was constructed and named 1A751/CTB-TEpiAs. Its capability to induce mucosal, humoral, and cellular responses in mice and guinea pigs was evaluated after oral administration with vegetative cells of 1A751/CTB-TEpiAs. In addition,

its capability to protect guinea pigs against homologous virus challenge was examined. All animals were given booster vaccination at day 21 after initial inoculation and guinea pigs were much challenged 3 weeks after booster vaccination. The control groups were inoculated with a commercial vaccine or administered orally with 1A751/pBC38C or an oral buffer. All animals vaccinated with 1A751/CTB-TEpiAs developed specific anti-FMDV IgA in lung and gut lavage fluid, serum ELISA antibody, neutralizing antibody as well as T lymphocyte proliferation, and IFN-gamma secretory responses. Three of the five guinea pigs vaccinated with 1A751/CTB-TEpiAs were protected completely from the viral challenge. The results demonstrate the potential viability of a B.