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Journal ArticleDOI

Localization of nitric oxide synthase indicating a neural role for nitric oxide

David S. Bredt, +2 more
- 25 Oct 1990 - 
- Vol. 347, Iss: 6295, pp 768-770
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TLDR
It is demonstrated that NO synthase in the brain to be exclusively associated with discrete neuronal populations, and prominent neural localizations provided the first conclusive evidence for a strong association of NO with neurons.
Abstract
Nitric oxide (NO), apparently identical to endothelium-derived relaxing factor in blood vessels, is also formed by cytotoxic macrophages, in adrenal gland and in brain tissue, where it mediates the stimulation by glutamate of cyclic GMP formation in the cerebellum Stimulation of intestinal or anococcygeal nerves liberates NO, and the resultant muscle relaxation is blocked by arginine derivatives that inhibit NO synthesis It is, however, unclear whether in brain or intestine, NO released following nerve stimulation is formed in neurons, glia, fibroblasts, muscle or blood cells, all of which occur in proximity to neurons and so could account for effects of nerve stimulation on cGMP and muscle tone We have now localized NO synthase protein immunohistochemically in the rat using antisera to the purified enzyme We demonstrate NO synthase in the brain to be exclusively associated with discrete neuronal populations NO synthase is also concentrated in the neural innervation of the posterior pituitary, in autonomic nerve fibres in the retina, in cell bodies and nerve fibres in the myenteric plexus of the intestine, in adrenal medulla, and in vascular endothelial cells These prominent neural localizations provide the first conclusive evidence for a strong association of NO with neurons

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Citations
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Journal ArticleDOI

BIdirectional Regulation of Neurogenesis by Neuronal Nitric Oxide Synthase Derived from Neurons and Neural Stem Cells

TL;DR: It is shown that nNOS from neural stem cells (NSCs) and from neurons play opposite role in regulating neurogenesis, and that NSCs‐derived nN OS stimulates neuroGenesis via activating telomerase, whereas neurons‐derived cAMP response element binding protein (CREB) phosphorylation, nNos expression, and proliferation are stimulated.
Journal ArticleDOI

Nitric oxide signaling in the retina: What have we learned in two decades?

TL;DR: The current state of knowledge on physiological NO signaling in the retina is analyzed and it is suggested that NO is a regulator of visual adaptation at different signal processing levels.
Journal ArticleDOI

Determination of kainic acid-induced release of nitric oxide using a novel hemoglobin trapping technique with microdialysis.

TL;DR: It is demonstrated that a microdialysis probe using a novel hemoglobin‐trapping technique possesses adequate sensitivity to determine the basal levels of NO and the ability of KA to increase these levels via a NO synthase‐mediated mechanism.
Journal ArticleDOI

Nitric oxide synthase is localized predominantly in the Golgi apparatus and cytoplasmic vesicles of vascular endothelial cells.

TL;DR: The presence of NOS in the Golgi apparatus and in vesicles raises the possibility that NOS may be exteriorized by endothelial cells, and hence that nitric oxide is synthesized extracellularly.
References
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Journal ArticleDOI

Isolation of nitric oxide synthetase, a calmodulin-requiring enzyme.

TL;DR: It is shown that nitric oxide synthetase activity requires calmodulin, and the native enzyme appears to be a monomer.

Isolation of nitric oxide synthetase, a calmodulin-requiring enzyme (endothelium-derived relaxing factor/arginine/cGMP)

TL;DR: In this paper, it was shown that NO synthetase is a calmodulin-requiring enzyme, and showed that NO formation is accompanied by the stoichiometric conversion of arginine to citrulline.
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Endothelium-derived relaxing factor release on activation of NMDA receptors suggests role as intercellular messenger in the brain.

TL;DR: It is reported here that by acting on NMDA (N-methyl-D-aspartate) receptors on cerebellar cells, glutamate induces the release of a diffusible messenger with strikingly similar properties to EDRF that accounts for the cGMP responses that take place following NMDA receptor activation.
Journal ArticleDOI

Endothelium-derived relaxing and contracting factors.

TL;DR: Endothelium-dependent relaxation of blood vessels is produced by a large number of agents (e.g., acetylcholine, ATP and ADP, substance P, bradykinin, histamine, thrombin, serotonin). With some agents, relaxation may be limited to certain species and/or blood vessels as mentioned in this paper.
Journal ArticleDOI

Nitric oxide mediates glutamate-linked enhancement of cGMP levels in the cerebellum

TL;DR: It is established that nitric oxide mediates the stimulation by glutamate of cGMP formation, which mediates influences of numerous neurotransmitters and modulators on vascular smooth muscle and leukocytes.
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