Evidence map›Paper›PMID 19005071›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Calcium-sensing receptor activation depresses synaptic transmission.

Cecilia G Phillips, Mark T Harnett, Wenyan Chen, Stephen M Smith

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Etiology and Pathophysiology of Hypoparathyroidism: A Narrative Review.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Pooled it
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  14. Distinct Actions of Voltage-Activated CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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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

4 authors at 2 institutions in 1 country.

Cecilia G PhillipsDivision of Pulmonary & Critical Care Medicine, Oregon Health & Science University, Portland, Oregon 97239, USA.
Mark T Harnett
Wenyan Chen
Stephen M Smith
Oregon Health & Science University · USPulmonary and Critical Care Associates · US

Funding

Nerve Terminal Regulation in the Cerebral CortexR01NS043444 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SMITH, STEPHEN M · 2003 to 2006
$1.0M
Howard Hughes Medical InstituteNINDS NIH HHS R01 NS043444NINDS NIH HHS R01-NS 43444
6 · The paper itself

Abstract

At excitatory synapses, decreases in cleft [Ca] arising from activity-dependent transmembrane Ca flux reduce the probability of subsequent transmitter release. Intense neural activity, induced by physiological and pathological stimuli, disturb the external microenvironment reducing extracellular [Ca] ([Ca](o)) and thus may impair neurotransmission. Increases in [Ca](o) activate the extracellular calcium sensing receptor (CaSR) which in turn inhibits nonselective cation channels at the majority of cortical nerve terminals. This pathway may modulate synaptic transmission by attenuating the impact of decreases in [Ca](o) on synaptic transmission. Using patch-clamp recording from isolated cortical terminals, cortical neuronal pairs and isolated neuronal soma we examined the modulation of synaptic transmission by CaSR. EPSCs were increased on average by 88% in reduced affinity CaSR-mutant (CaSR(-/-)) neurons compared with wild-type. Variance-mean analysis indicates that the enhanced synaptic transmission was due largely to an increase in average probability of release (0.27 vs 0.46 for wild-type vs CaSR(-/-) pairs) with little change in quantal size (23 +/- 4 pA vs 22 +/- 4 pA) or number of release sites (11 vs 13). In addition, the CaSR agonist spermidine reduced synaptic transmission and increased paired-pulse depression at physiological [Ca](o). Spermidine did not affect quantal size, consistent with a presynaptic mechanism of action, nor did it affect voltage-activated Ca channel currents. In summary, reduced CaSR function enhanced synaptic transmission and CaSR stimulation had the opposite effect. Thus CaSR provides a mechanism that may compensate for the fall in release probability that accompanies decreases in [Ca](o).

Indexed as

AnimalsCalciumCalcium SignalingCells, CulturedCerebral CortexDown-RegulationExcitatory Postsynaptic PotentialsMiceMice, KnockoutNeural InhibitionNeuronal PlasticityNeuronsOrgan Culture TechniquesPatch-Clamp TechniquesPresynaptic TerminalsReceptors, Calcium-SensingCalciumReceptors, Calcium-SensingSpermidine

Identifiers

PMID19005071
PMCPMC2761683
OpenAlexW1996382370

What OpenQuestion holds

Textmetadata
LicenceTDM
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.