Evidence map›Paper›PMID 18588525›Full record

ReviewThe European journal of neuroscience2008

Concepts of neural nitric oxide-mediated transmission.

John Garthwaite

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The European journal of neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 336 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
336citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

336 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  15. Gasotransmitters in Glaucoma: A New Paradigm.Bulletin of pharmaceutical research · 2026
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276 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

John GarthwaiteWolfson Institute for Biomedical Research, University College London, Gower Street, London WCIE 6BT, UK. john.garthwaite@ucl.ac.uk

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research CouncilWellcome Trust
6 · The paper itself

Abstract

As a chemical transmitter in the mammalian central nervous system, nitric oxide (NO) is still thought a bit of an oddity, yet this role extends back to the beginnings of the evolution of the nervous system, predating many of the more familiar neurotransmitters. During the 20 years since it became known, evidence has accumulated for NO subserving an increasing number of functions in the mammalian central nervous system, as anticipated from the wide distribution of its synthetic and signal transduction machinery within it. This review attempts to probe beneath those functions and consider the cellular and molecular mechanisms through which NO evokes short- and long-term modifications in neural performance. With any transmitter, understanding its receptors is vital for decoding the language of communication. The receptor proteins specialised to detect NO are coupled to cGMP formation and provide an astonishing degree of amplification of even brief, low amplitude NO signals. Emphasis is given to the diverse ways in which NO receptor activation initiates changes in neuronal excitability and synaptic strength by acting at pre- and/or postsynaptic locations. Signalling to non-neuronal cells and an unexpected line of communication between endothelial cells and brain cells are also covered. Viewed from a mechanistic perspective, NO conforms to many of the rules governing more conventional neurotransmission, particularly of the metabotropic type, but stands out as being more economical and versatile, attributes that presumably account for its spectacular evolutionary success.

Indexed as

AnimalsCell CommunicationEvolution, MolecularFeeding BehaviorHumansNervous SystemNeuronsNitric OxideReceptors, G-Protein-CoupledSignal TransductionSynaptic TransmissionNitric OxideReceptors, G-Protein-Coupled

Identifiers

PMID18588525
PMCPMC2610389

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.