Evidence map›Paper›PMID 25859184›Full record

ArticleFrontiers in cellular neuroscience2015

A single-cross, RNA interference-based genetic tool for examining the long-term maintenance of homeostatic plasticity.

Douglas J Brusich, Ashlyn M Spring, C Andrew Frank

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

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  17. A Screen for Synaptic Growth Mutants Reveals Mechanisms That Stabilize Synaptic Strength.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  18. Endogenous Tagging Reveals Differential Regulation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  19. Article
  20. Comprehensive Modeling of Spinal Muscular Atrophy inFrontiers in molecular neuroscience · 2019
    Article
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

3 authors at 1 institution in 1 country.

Douglas J BrusichDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa Iowa City, IA, USA.
Ashlyn M SpringDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa Iowa City, IA, USA ; Interdisciplinary Graduate Program in Genetics, University of Iowa Iowa City, IA, USA.
C Andrew FrankDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa Iowa City, IA, USA ; Interdisciplinary Programs in Genetics, Neuroscience, and MCB, University of Iowa Iowa City, IA, USA.
University of Iowa · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008629 · NIGMS · UNIVERSITY OF IOWA · PI EBERL, DANIEL F · 1997 to 2021
$4.1M
How Ephexin Signaling Promotes Neuronal StabilityR00NS062738 · NINDS · UNIVERSITY OF IOWA · PI FRANK, CARL ANDREW · 2010 to 2012
$725k
How Ephexin Signaling Promotes Neuronal StabilityK99NS062738 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FRANK, CARL ANDREW · 2008 to 2009
$171k
NIGMS NIH HHS T32 GM008629NINDS NIH HHS K99 NS062738NINDS NIH HHS R00 NS062738
6 · The paper itself

Abstract

Homeostatic synaptic plasticity (HSP) helps neurons and synapses maintain physiologically appropriate levels of output. The fruit fly Drosophila melanogaster larval neuromuscular junction (NMJ) is a valuable model for studying HSP. Here we introduce a genetic tool that allows fruit fly researchers to examine the lifelong maintenance of HSP with a single cross. The tool is a fruit fly stock that combines the GAL4/UAS expression system with RNA interference (RNAi)-based knock down of a glutamate receptor subunit gene. With this stock, we uncover important new information about the maintenance of HSP. We address an open question about the role that presynaptic CaV2-type Ca(2+) channels play in NMJ homeostasis. Published experiments have demonstrated that hypomorphic missense mutations in the CaV2 α1a subunit gene cacophony (cac) can impair homeostatic plasticity at the NMJ. Here we report that reducing cac expression levels by RNAi is not sufficient to impair homeostatic plasticity. The presence of wild-type channels appears to support HSP-even when total CaV2 function is severely reduced. We also conduct an RNAi- and electrophysiology-based screen to identify new factors required for sustained homeostatic signaling throughout development. We uncover novel roles in HSP for Drosophila homologs of Cysteine string protein (CSP) and Phospholipase Cβ (Plc21C). We characterize those roles through follow-up genetic tests. We discuss how CSP, Plc21C, and associated factors could modulate presynaptic CaV2 function, presynaptic Ca(2+) handling, or other signaling processes crucial for sustained homeostatic regulation of NMJ function throughout development. Our findings expand the scope of signaling pathways and processes that contribute to the durable strength of the NMJ.

Indexed as

CaV2 channelscysteine string proteinDrosophila melanogasterhomeostatic plasticityneuromuscular junctionphospholipase C betaRNAi screeningsynaptic transmission

Identifiers

PMID25859184
PMCPMC4374470
OpenAlexW1995764961

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.