TY - JOUR
T1 - Mechanisms of M1 muscarinic receptor-mediated up-regulation of neuronal nitric oxide synthase in N1E-115 neuroblastoma cells
AU - Cuadra, Adolfo E.
AU - El-Fakahany, Esam E.
N1 - Funding Information:
This work was supported by NIH grant NS25743 (EEE) and its supplement (EAC).
PY - 2005/4/4
Y1 - 2005/4/4
N2 - The neuronal form of nitric oxide synthase (nNOS) was generally assumed to be constitutively expressed at a constant level. However, it is now becoming recognized that its expression can be modulated by a number of physiological and pathophysiological conditions. Previously, we reported that nNOS expression is up-regulated after prolonged muscarinic M1 receptor stimulation. In this work, we report that muscarinic receptor activation signals the up-regulation of nNOS via multiple pathways in N1E-115 mouse neuroblastoma cells. These include protein kinase C (PKC) activation, cytosolic calcium mobilization and NO production. Further characterization showed that the half-life of nNOS is slightly, but significantly, increased in agonist-pretreated cells compared with vehicle-treated control cells. Based on these data, it appears that the level of nNOS expression is modulated in a complex manner by a number of mechanisms that include, but might not be limited to, those described here.
AB - The neuronal form of nitric oxide synthase (nNOS) was generally assumed to be constitutively expressed at a constant level. However, it is now becoming recognized that its expression can be modulated by a number of physiological and pathophysiological conditions. Previously, we reported that nNOS expression is up-regulated after prolonged muscarinic M1 receptor stimulation. In this work, we report that muscarinic receptor activation signals the up-regulation of nNOS via multiple pathways in N1E-115 mouse neuroblastoma cells. These include protein kinase C (PKC) activation, cytosolic calcium mobilization and NO production. Further characterization showed that the half-life of nNOS is slightly, but significantly, increased in agonist-pretreated cells compared with vehicle-treated control cells. Based on these data, it appears that the level of nNOS expression is modulated in a complex manner by a number of mechanisms that include, but might not be limited to, those described here.
KW - Cellular homeostasis
KW - Enzyme expression
KW - Signal transduction
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U2 - 10.1016/j.molbrainres.2004.10.022
DO - 10.1016/j.molbrainres.2004.10.022
M3 - Article
C2 - 15836917
AN - SCOPUS:17044410071
SN - 0169-328X
VL - 134
SP - 198
EP - 204
JO - Molecular Brain Research
JF - Molecular Brain Research
IS - 2
ER -
