Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.
Optogenetic experiments show that bridging microtubules buffer chromosome movements and promote their alignment through forces transferred to the associated kinetochore fibers, which rely on precise regulation of the overlap region.
Electrophysiological and simulation approaches show that a chloride-related longer relaxation of the inhibitory synaptic events partially compensates the early defect in the chloride homeostasis detected in fetal SOD spinal motoneurons.
A cationic molecule derived from an uncharged Cav2.2 calcium channel inhibitor powerfully inhibits both sodium and calcium channels with extracellular application and inhibits both pain and neurogenic inflammation.
Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.