Stress-induced sleep-like inactivity modulates stress susceptibility in mice.

Severe environmental and social stress induces dysregulation of sleep along with mood and cognitive disturbances. However, the role and mechanism of this sleep dysregulation remain elusive. Here we evaluated sleep-like inactivity measured by voluntary movements and its relationship to social behaviors in mice without or with social defeat stress as well as the stressed mice with subsequent sleep deprivation.

Social defeat stress-specific increase in c-Fos expression in the extended amygdala in mice: Involvement of dopamine D1 receptor in the medial prefrontal cortex.

We recently reported that dopamine D1 receptor in the medial prefrontal cortex (mPFC) is activated by subthreshold social defeat stress and suppresses the induction of depressive-like behavior in mice. However, which mPFC projection(s) mediates this antidepressant-like effect remains poorly understood. Here we show that social defeat stress specifically increased c-Fos expression, a marker for neuronal activity, in distinct brain regions involved in emotional regulation, relative to novelty-induced exploration.

Social defeat stress induces phosphorylation of extracellular signal-regulated kinase in the leptomeninges in mice.

Aims: Animal studies using various stress models have shown that excessive environmental stress induces depression? and anxiety?like behaviors through inflammatory responses in the brain and periphery. Although the leptomeningeal cells have multiple functions related to inflammatory responses in the brain, whether environmental stress influences the leptomeninges remains unknown. In this study, we aimed to examine phosphorylation of the extracellular signal-regulated kinase (ERK) in the leptomeninges.

Differential -palmitoylation of the human and rodent β-adrenergic receptors.

With few reported exceptions, G protein-coupled receptors (GPCRs) are modified by Cys palmitoylation (-palmitoylation). In multiple GPCRs, -palmitoylation targets a canonical site within the C-terminal cytoplasmic tail adjacent to the C terminus of the seventh transmembrane domain, but modification of additional sites is exemplified by the β-adrenergic receptors (βARs). The βAR is -palmitoylated at a second, more distal site within the C-terminal tail, and the βAR is modified at a second site within the third intracellular loop, neither of which is conserved in other βAR isoforms.