Research progress on neurobiology of neuronal nitric oxide synthase

摘要: Neuronal nitric oxide synthase (nNOS) is mainly expressed in neurons, to some extent astrocytes and neuronal stem cells. The alternative splicing of nNOS mRNA generates 5 isoforms nNOS, including nNOS-α, nNOS-β, nNOS-μ, nNOS-γ nNOS-2. Monomer inactive, dimer the active form. Dimerization requires tetrahydrobiopterin (BH4), heme L-arginine binding. Regulation expression relies largely on cAMP response element-binding protein (CREB) activity, activity regulated by heat shock 90 (HSP90)/HSP70, calmodulin (CaM), phosphorylation dephosphorylation at Ser847 Ser1412, inhibitor (PIN). There are primarily 9 nNOS-interacting proteins, post-synaptic density 95 (PSD95), clathrin assembly lymphoid leukemia (CALM), calcium/calmodulindependent kinase II alpha (CAMKIIA), Disks large homolog 4 (DLG4), DLG2, 6-phosphofructokinase, muscle type (PFK-M), carboxy-terminal PDZ ligand (CAPON) protein, syntrophin dynein light chain (LC). Among them, PSD95, CAPON PFK-M important adapter proteins neurons. interaction PSD95 with controls synapse formation implicated N-methyl-D-aspartic acid-induced death. nNOS-derived NO loss-mediated early cognitive/motor deficits several neuropathological states, negatively regulates neurogenesis under physiological pathological conditions.