scispace - formally typeset
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
Reads0
Chats0
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

read more

Citations
More filters
Journal ArticleDOI

Role of No production in NMDA receptor-mediated neurotransmitter release in cerebral cortex

TL;DR: Results suggest that NO production and its extracellular movement may be links in the pathway from NMDA receptor activation to changes in chemical signaling in surrounding synaptic terminals in the cerebral cortex.
Journal ArticleDOI

NO as a signalling molecule in the nervous system

TL;DR: There is growing evidence that nNOS biosynthesis in excitable tissues is not restricted to neurones while substantial amounts of this enzyme have been identified in skeletal muscle, where it is involved in the regulation of metabolism and muscle contractility.
Journal ArticleDOI

Long-term synaptic depression in the mammalian brain

TL;DR: This review shall examine the opposite phenomenon, use-dependent decreases in synaptic strength, or long-term depression, which is a broad term that is used to describe synaptic depression according to several different learning rules and in a wide variety of brain structures.
Journal ArticleDOI

New roles for glia

TL;DR: Findings indicate that glial cells can sense, and potentially respond to, a large array of neuronal signals and neurobiologists should reconsider the possible significance of active neuronal-glial signaling.
Journal ArticleDOI

Regulation of the cerebral microcirculation during neural activity: is nitric oxide the missing link?

TL;DR: Evidence that nitric oxide participates in the maintenance of resting cerebral blood flow and in the cerebrovasodilatation elicited by increased neural activity is critically reviewed and discussed in the context of general principles of cerebrovascular regulation.
References
More filters
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.
Journal ArticleDOI

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.
Related Papers (5)