At the molecular Fedratinib cell line and cellular level, both drugs have very different mechanisms of action. Nicotine specifically activates ligand-gated ion channels in the brain, which are normally gated by acetylcholine, while alcohol interacts with various neurotransmitter receptors. Despite this diversity, both drugs seem to engage the endogenous opioid system as a modulator of some of its pharmacological effect. An acute exposure to nicotine or alcohol leads to a release of opioid peptides in specific brain regions, thus resulting in an activation of their corresponding receptors. If the brain is exposed repeatedly or chronically to these drugs, adaptive

changes in the Acalabrutinib cost level and expression of opioid peptides and receptors occur. These adaptive changes are thought to contribute to the homeostatic or allostatic adaptations of the brain, which have been associated with drug dependence. This review summarizes pharmacological and genetic studies in animal models and in humans that have addressed the role of specific opioid peptides and receptors in various stages of the addiction process. (C) 2009 Published by Elsevier Ltd.”
“Models

describing the neural correlates of biased emotion processing in depression have focused on increased activation of anterior cingulate and amygdala and decreased activation of striatum and dorsolateral prefrontal cortex. However, neuroimaging studies investigating emotion processing in depression have reported inconsistent results. This meta-analysis integrates these findings and examines whether emotional valence modulates such abnormalities. A systematic literature search identified 26 whole-brain and 18 region-of-interest studies. Peak coordinates and effect sizes were combined in an innovative parametric meta-analysis. Opposing effects were observed in the amygdala, striatum, parahippocampal, cerebellar, fusiform and anterior cingulate cortex, with depressed subjects displaying hyperactivation for negative stimuli and hypoactivation for positive

stimuli. Anterior cingulate activity was also modulated by facial versus non-facial stimuli, selleckchem in addition to emotional valence. Depressed subjects also showed reduced activity in left dorsolateral prefrontal cortex for negative stimuli and increased activity in orbitofrontal cortex for positive stimuli. Emotional valence is a moderator of neural abnormalities in depression, and therefore a critical feature to consider in models of emotional dysfunction in depression. (C) 2012 Elsevier Ltd. All rights reserved.”
“This article aims at making readers, experimentalists and theorists, more aware of the abstractions made by an observer when measuring and reporting behavioral and neural timescales.