Activation of G protein-coupled C188-9 molecular weight receptors can transiently inhibit vesicular release through the release of G beta gamma which binds to both voltage-dependent calcium channels to reduce calcium influx, and directly to the C-terminus region of the SNARE protein SNAP-25. Our recent work has revealed that the binding of G beta gamma to SNAP-25 is necessary, but not sufficient, to elicit long-term depression (LTD) of vesicular glutamate release, and that the concomitant release of G alpha(i) and the second messenger nitric oxide are also necessary steps in the presynaptic LTD cascade. Here, we review the current state of knowledge of the

molecular steps mediating short-term and long-term plasticity of vesicular release at glutamatergic synapses, and the many gaps that remain to be addressed.

This article is part of a Special Issue entitled ‘Metabotropic Glutamate Receptors’. (c) 2012 Elsevier Ltd. All rights reserved.”
“Numerous social-cognitive models posit that social behavior largely is driven by links between constructs in long-term memory that automatically become activated when relevant stimuli are encountered. Various response biases have

been understood in terms of the influence of such “”implicit”" processes on behavior. This article selleckchem reviews event-related potential (ERP) studies investigating the role played by cognitive control and conflict resolution processes in social-cognitive phenomena typically deemed automatic. Neurocognitive responses associated with response activation and conflict often are sensitive to the same stimulus manipulations that produce differential behavioral responses on RAS p21 protein activator 1 social-cognitive tasks and that often are attributed to the role of automatic associations. Findings are discussed in the context of an overarching social cognitive neuroscience model in which physiological data are used to constrain

social-cognitive theories.”
“Major depressive disorder is among the most prevalent forms of mental illness. All currently available antidepressant medications have stemmed from study of the mechanisms of serendipitously discovered drugs, and only 30-50% of patients exhibit remission and frequently at least 3-4 weeks are required for manifestation of significant therapeutic effects. To overcome these drawbacks, discovering novel neuronal mechanisms of pathophysiology of depression as well as more effective treatments are necessary. This review focuses on the metabotropic glutamate (mGlu) receptors and their potential for drug targets for the treatment of depression. In particular, accumulating evidence has indicated the potential importance and usefulness of agents acting on mGlu2/3 and mGlu5 receptors. Preclinical and clinical evidence of mGlu2/3 receptor ligands and mGlu5 receptor antagonists are described.