Nitric oxide synthase in the peripheral nervous system of the goldfish, Carassius auratus

1996 ◽  
Vol 284 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Gerold Brüning ◽  
Katharina Hattwig ◽  
Bernd Mayer
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Peripheral Nervous System ◽  
Carassius Auratus ◽  
Goldfish Carassius Auratus ◽  
Oxide Synthase

Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system

2001 ◽  
Vol 120 (5) ◽  
pp. A176-A176
Author(s):  
P KOPPITZ ◽  
M STORR ◽  
D SAUR ◽  
M KURJAK ◽  
H ALLESCHER
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Inhibitory Effect ◽  
Oxide Synthase

scholarly journals Modulation of Opioid Actions by Nitric Oxide Signaling

2009 ◽  
Vol 110 (1) ◽  
pp. 166-181 ◽  
Author(s):  
Noboru Toda ◽  
Shiroh Kishioka ◽  
Yoshio Hatano ◽  
Hiroshi Toda ◽  
David S. Warner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Glial Cells ◽  
Withdrawal Syndrome ◽  
Therapeutic Agents ◽  
Nitric Oxide Signaling ◽  
Endogenous Nitric Oxide ◽  
Oxide Synthase ◽  
New Strategies

Nitric oxide (NO) plays pivotal roles in controlling physiological functions, participates in pathophysiological intervention, and is involved in mechanisms underlying beneficial or untoward actions of therapeutic agents. Endogenous nitric oxide is formed by three isoforms of nitric oxide synthase: endothelial, neurogenic and inducible. The former two are constitutively present mainly in the endothelium and nervous system, respectively, and the latter one is induced by lipopolysaccharides or cytokines mainly in mitochondria and glial cells. Constitutively formed nitric oxide modulates the actions of morphine and related analgesics by either enhancing or reducing antinociception. Tolerance to and dependence on morphine or its withdrawal syndrome are likely prevented by nitric oxide synthase inhibition. Information concerning modulation of morphine actions by nitric oxide is undoubtedly useful in establishing new strategies for efficient antinociceptive treatment and for minimizing noxious and unintended reactions.

scholarly journals Transplantation of enteric nervous system stem cells rescues nitric oxide synthase deficient mouse colon

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Conor J. McCann ◽  
Julie E. Cooper ◽  
Dipa Natarajan ◽  
Benjamin Jevans ◽  
Laura E. Burnett ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stem Cells ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Deficient Mouse ◽  
Mouse Colon ◽  
Oxide Synthase

scholarly journals Perinatal Lead Exposure Alters the Expression of Neuronal Nitric Oxide Synthase in Rat Brain

2001 ◽  
Vol 20 (3) ◽  
pp. 113-120 ◽  
Author(s):  
C. S. Chetty ◽  
G. R. Reddy ◽  
K. S. Murthy ◽  
J. Johnson ◽  
K. Sajwan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Enzyme Activity ◽  
Nitric Oxide Synthase ◽  
Rat Brain ◽  
Cognitive Deficits ◽  
Neuronal Nitric Oxide Synthase ◽  
Pb Exposure ◽  
Oxide Synthase ◽  
Developing Nervous System

Environmental exposure to lead (Pb) is known to affect the developing nervous system causing cognitive deficits in children. The diffusible nitric oxide (NO) is a biological messenger known to be involved in brain development. We examined the developmental changes of neuronal nitric oxide synthase (nNOS) in cerebellum and hippocampus of developing rat brain by radiometric assay, Western blot analysis and immunohistochemistry. Pb-exposure (0.2% Pb acetate) was initiated on gestation day 6 through the drinking water of the dam and continued through birth and postnatal days (PNDs) 1 to 21. The pups were never exposed to Pb directly. Pb exposure was stopped on weaning of pups from mothers on PND 21. The changes in nNOS were measured in the offspring on PNDs 7, 14, 21, and 35. The nNOS activity was increased gradually from PNDs 7 to 35 in both cerebellum and hippocampus of control rats when the enzyme activity was determined in the presence of either 0.5 or 6 μM calcium (Ca2+) in the reaction mixture. However, Pb exposure decreased the nNOS activity significantly at PNDs 21 to 35 as compared to respective controls when the enzyme activity was determined in the presence of 6 μM Ca2+. The decrease of nNOS was even greater and evident at all PNDs tested when the enzyme activity was assayed in the presence of physiological concentration of Ca2+ (0.5 μM). These findings were further strengthened by the in vitro studies. The cerebellar nNOS activity was inhibited much more at low Ca2+ (0.5 μM) as compared to 6 μM Ca2+, with IC50 values of 35 and 50 nM Pb, respectively. The nNOS protein levels and immunoreactivity in the cerebellum and hippocampus of rats perinatally exposed to Pb were decreased as compared to controls at PNDs 21 and 35. These data suggest perinatal Pb exposure decreases the nNOS in the developing brain. The decrease of nNOS activity and protein may explain the Pb-mediated cognitive deficits because NO regulates long-term potentiation (LTP) and other neurophysiological events in the developing nervous system.

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