Evidence map›Paper›PMID 17959793›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Cell-autonomous inhibition of alpha 7-containing nicotinic acetylcholine receptors prevents death of parasympathetic neurons during development.

Martin Hruska, Rae Nishi

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

16 citing papers in PubMed, 29 citations in OpenAlex.

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  8. A dominant mutation in a neuronal acetylcholine receptor subunit leads to motor neuron degeneration in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
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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

2 authors at 1 institution in 1 country.

Martin HruskaDepartment of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington, Vermont 05405, USA.
Rae Nishi
University of Vermont · US

Funding

Proteomics Core for Neuroscience P20 RR16435P20RR016435 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI SPEES, JEFFREY L · 2001 to 2010
$23.5M
MECHANISMS OF TROPHIC MOLECULES IN NEURONAL DEVELOPMENTR01NS025767 · NINDS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NISHI, RAE · 1989 to 2005
$2.0M
Nicotinic Acetylcholine Receptors in Neural DevelopmentR01DA017784 · NIDA · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NISHI, RAE · 2005 to 2009
$1.6M
NCRR NIH HHS P20 RR016435NCRR NIH HHS P20 RR16435NIDA NIH HHS DA017784NIDA NIH HHS R01 DA017784NINDS NIH HHS NS25767NINDS NIH HHS R01 NS025767
6 · The paper itself

Abstract

Neurotrophic molecules are key retrograde influences of cell survival in the developing nervous system, but other influences such as activity are also emerging as important factors. In the avian ciliary ganglion, half the neurons are eliminated between embryonic day 8 (E8) and E14, but it is not known how cell death is initiated. Because systemic application of alpha7-nicotinic acetylcholine receptor (nAChR) antagonists prevents this cell loss, we examined differences in receptor densities and responses of intracellular calcium to nicotine using the calcium-sensitive dye fura-2. In addition, we determined whether cell-autonomous inhibition of alpha7 activation in neurons prevented cell death. E8 neurons are heterogeneous with respect to alpha7-nAChR density, which leads to large increases in [Ca2+]i in some neurons; E8 neurons also exhibit a slower rate of Ca2+ decay after nicotinic stimulation than E13 neurons. Expressing alpha-bungarotoxin that is tethered to the membrane by a glycosylphosphatidylinositol linkage (GPIalpha btx) in ciliary ganglion neurons with the retroviral vector RCASBP(A) blocks increases in intracellular calcium induced by nicotine through alpha7-nAChRs and prevents neurons from dying. Expression of GPIalpha btx in surrounding non-neural tissues, but not in neurons, does not prevent cell loss. Furthermore, the GPIalpha btx is not efficiently expressed in the accessory oculomotor neurons, eliminating preganglionic inputs as another site for action of the antagonist. These results support the hypothesis that cholinergic inputs facilitate cell death in the developing autonomic nervous system by activating alpha7-nAChRs, possibly by leading to increases in intracellular calcium that exceed the threshold for cell survival.

Indexed as

Adrenergic alpha-Antagonistsalpha7 Nicotinic Acetylcholine ReceptorAnimalsCell DeathChick EmbryoCiliary BodyGanglia, ParasympatheticNeural InhibitionNeuronsReceptors, NicotinicAdrenergic alpha-Antagonistsalpha7 Nicotinic Acetylcholine ReceptorReceptors, Nicotinic

Identifiers

PMID17959793
PMCPMC2919487
OpenAlexW2051606999

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.