Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum.

ABSTRACT: Nitric oxide (NO) is a major inhibitory neurotransmitter that mediates nonadrenergic noncholinergic (NANC) signaling. Neuronal NO synthase (nNOS) is activated by Ca²⁺/calmodulin to produce NO, which causes smooth muscle relaxation to regulate physiologic tone. nNOS serine1412 (S1412) phosphorylation may reduce the activating Ca²⁺ requirement and sustain NO production. We developed and characterized a nonphosphorylatable nNOS^S1412A knock-in mouse and evaluated its enteric neurotransmission and gastrointestinal (GI) motility to understand the physiologic significance of nNOS S1412 phosphorylation. Electrical field stimulation (EFS) of wild-type (WT) mouse ileum induced nNOS S1412 phosphorylation that was blocked by tetrodotoxin and by inhibitors of the protei

SUBMITTER: Guerra DD 

PROVIDER: S-EPMC6717252 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature