Galaxies in voids assemble their stars slowly.

Galaxies in the Universe are distributed in a web-like structure characterized by different large-scale environments: dense clusters, elongated filaments, sheetlike walls and under-dense regions, called voids. The low density in voids is expected to affect the properties of their galaxies. Indeed, previous studies have shown that galaxies in voids are, on average, bluer and less massive, and have later morphologies and higher current star formation rates than galaxies in denser large-scale environments.

-Acetyl β-Endorphin Is an Endogenous Ligand of σ1Rs That Regulates Mu-Opioid Receptor Signaling by Exchanging G Proteins for σ2Rs in σ1R Oligomers.

The opioid peptide β-endorphin coexists in the pituitary and brain in its -acetylated form, which does not bind to opioid receptors. We now report that these neuropeptides exhibited opposite effects in in vivo paradigms, in which ligands of the sigma type 1 receptor (σ1R) displayed positive effects. Thus, -acetyl β-Endorphin reduced vascular infarct caused by permanent unilateral middle cerebral artery occlusion and diminished the incidence of -methyl-D-aspartate acid-promoted convulsive syndrome and mechanical allodynia caused by unilateral chronic constriction of the sciatic nerve.

The sigma-1 receptor curtails endogenous opioid analgesia during sensitization of TRPV1 nociceptors.

Background And Purpose: Peripheral sensitization contributes to pathological pain. While prostaglandin E2 (PGE2) and nerve growth factor (NGF) sensitize peptidergic C-nociceptors (TRPV1+), glial cell line-derived neurotrophic factor (GDNF) sensitizes non-peptidergic C-neurons (IB4+). The sigma-1 receptor (sigma-1R) is a Ca -sensing chaperone known to modulate opoid analgesia.

The σ1 Receptor and the HINT1 Protein Control α2δ1 Binding to Glutamate NMDA Receptors: Implications in Neuropathic Pain.

Nerve injury produces neuropathic pain through the binding of α2δ1 proteins to glutamate -methyl-D-aspartate receptors (NMDARs). Notably, mice with a targeted deletion of the sigma 1 receptor ( gene do not develop neuropathy, whereas mice lacking the histidine triad nucleotide-binding protein 1 ( gene exhibit exacerbated allodynia. σ1R antagonists more effectively diminish neuropathic pain of spinal origin when administered by intracerebroventricular injection than systemically.

Effects of Gαi and Gαz protein knockdown on alpha-adrenergic and cannabinoid CB receptor regulation of MEK-ERK and FADD pathways in mouse cerebral cortex.

Background: Alpha-adrenergic (α-AR) and cannabinoid CB (CB-R) receptors exert their functions modulating multiple signaling pathways, including MEK-ERK (extracellular signal-regulated kinases) and FADD (Fas-associated protein with death domain) cascades. These molecules are relevant in finding biased agonists with fewer side effects, but the mechanisms involving their modulations by α-AR- and CB-R in vivo are unclear. This study investigated the roles of Gαi and Gαz proteins in mediating α-AR- and CB-R-induced alterations of MEK-ERK and FADD phosphorylation (p-) in mouse brain cortex.